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127 Cards in this Set
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CRYSTALS FOUND IN SYNOVIAL FLUID:
Monosodium Urate - monohydrate Calcium - pyrophosphate - dihydrate |
Acute Gout
Tophaceous Gout Asymptomatic Acute Pseudogout Destructive Arthropathy Asx |
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Basic Calcium
- Phosphate Calcium Oxalate Lipid Cholesterol |
Acute Calcific Periarthritis
Acute Arthritis Destructive Arthropathy (Milwaukee Shoulder/Knee) Acute, Subacute Arthritis Asx Acute Arthritis Asx |
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Joint morning stiffness >1 hour
Simultaneous involvement (swelling) of >3 joints observed by a physician (PIP, MCP, wrist, knee, elbow, ankle, MTP) Hand involvement Symmetrical involvement Rheumatoid nodules + Rheumatoid factor X-ray changes (erosions or juxtaarticular osteopenia) |
Criteria for Classification of RA
must have 4 persisting for >6 wks |
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RA Epidemiology:
US frequency 1% but up to 2-3% in older person Female to male 2:1 Increased frequency in ____________(5-7%) Onset from _______ 70 to 80% +___ 1.5 to 2 fold increase in frequency if there is a _____________ afflicted |
Native Americans
30-50 RF first degree relative |
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High specificity autoantibodies have been described in the sera of RA patients
proven 98% specific to RA |
Anti-CCP antibodies
always treat if + because w/in 5 yrs will have gross deformities |
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Less specific than RF and CCP
Useful in distinguishing RA from noninflammatory conditions e.g. OA/FMS Can be used to monitor disease activity. |
Acute phase reactants (ESR & CRP)
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Key features:
Painful inflammation with tenderness on applied pressure to joint, or by moving joint. Swelling due to synovial hypertrophy or effusion |
RA
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RA Hand Findings:
MCP and PIP involvement is typical ____ and ____ MCP present 1st PIP ROM less than ____ degrees. MCP rom less than ___ degrees. Thickening of the _________ Nodulosis along tendon sheaths Decreased ______ strength Ulnar drift, boutenniere changes, swan neck changes |
2nd and 3rd
120 90 tendon sheaths grip |
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RA Upper Limb findings
_______ is most commonly involved. (loss of extension/flexion), radial drift causes ____________ prominence ________ - loss of extension (fixed flexion). Most common site of nodules _________ disease is a late finding with rare effusions occuring. |
Wrist
ulnar styloid Elbow Shoulder |
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RA Lower Limb Findings:
Tenderness of ____ Erosive damage causes _________ drift of toes Ankle RA causes swelling at the __________ joint (usually wrongly diagnsoed as edema or cellulitis). Also impinges p. tibial n causing _________ |
MTP
lateral tibiotalar paresthesia |
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RA Knee & Hip involvement:
__________ of the knee is most common. __________ of the knee is usually limited __________ formation common, always assess for rupture (_________ sign at l. malleolus). Erosions can occur at femoral condyles, tibial plateau causing varus or valgus changes. ______ - Pain in groin, thigh, low back, or referred to knee is common with effusion/involvement |
Effusion
Flexion Bakers cyst crescent Hips |
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RA Atlanto-Axial Subluxation:
Potentially a neurosurgical emergency Occurs in patients with _________ at onset of RA, more active _________ and rapidly progressive erosive peripheral disease Approximately 50-60% of RA patients referred for ____ or ____ will have radiographic evidence of subluxation Inquire about neck pain and neurological symptoms (painless sensory loss in extremities, “drop attacks,” unexplained weakness) Pre-op C-spine XR (flexion-extension views) in general anesthesia Look for > ____ separation between the odontoid process and the C1 arch in flexion 5-year mortality rate for patients with cervical subluxation with or without neurologic symptoms is 17% |
older age
synovitis TKR or THR 3mm |
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RA Cricoarytenoid Joint:
Common in 30% of RA patients Presents as ___________ and _____________ stridor |
hoarseness
inspiratory |
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RA DDx:
______________: rubella, Parvo, hep B can cause polyarthritis from weeks to months. Other CT diseases & ___________: usually hard to differentiate early on, but long standing RA will stand out with the am stiffness persisting, symmetry, nodules, and deformities. Also, SLE arthritis is reducible deformities Hypermobility and ___________: absence of serologies, ESR/CRP ____________: always high on differential with monoarthritis presentation. Must have other features e.g. urethritis, enteric infection, heel pain, sacroilitis on xray, + HLaB27. ReA is assymetrical, rare a.m. stiffness, rare RF or CCP positivitiy. characteristic ‘sausage’ dactylitis. |
Acute viral polyarthritis
Sarcoidosis Fibromyalgia Sx Reactive Arthritis |
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RA DDx (cont):
____ - DIP predominance with hard bony heberdeen and bouchard changes. _____: extremely similar, usually only distinguishing feature is fam hx, skin psoriasis, nail changes, dactylitis. ____________ arthropathy: gout, oxylate, uric acid _____________: ruled out with aspiration of the joint, culture A.M. stiffness generally less than 10 minutes Narrowing of joint spaces on xray vs. erosion No associated RF, CCP ab, ESR, CRP |
OA
PsA Crystalline Infectious arthritis |
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RA Non Disease Modifiers
Analgesics: 1. OTC ________, Pain meds: tramadol, topical steroid creams, hydrocodone. 2. _______: provide analgesia and anti-inflammatory response. Ex. Celebrex, Mobic. 3. ____________: Provide the most rapid response with pain relief and antiinflammatory response |
Tylenol
NSAIDS Glucocorticoids |
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________: Have the potential to reduce or prevent joint damage, preserve joint integrity and function, reduce health costs, and maintain economic productivity
Types used today: Early DMARDS, AntiCytokine Therapies, Biologics |
DMARDS
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Early Use DMARDS
1. _________/___________– more European than US. (100 mg bid) 2. ___________(hydroxychloroquine) 200mg bid 3. __________ (sulfasalazine) 500 mg 1-2 bid 4. _______(lefluonomide) 10-20mg qd as tolerated 5. ____________ 5-20mg once weekly 6. _________ (azathioprine) 50mg 1-2 po bid |
Doxycycline/Minocycline
Plaquenil Azulfidine Arava *Methotrexate* Imuran |
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There is little conclusive evidence that there is sustained benefit from step-up, step-down, or parallel use of traditional small molecule DMARDs in combinations, unless ___________ is included in the regimen
A combination of methotrexate with an _____________ is often effective in reducing disease activity and reducing the rate of radiographic progression of joint disease |
methotrexate
anti-TNF agent |
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Anti-Tumor Necrosis Factor Alpha
________(etanercept) 50mg sq once weekly. ________ (adalimumab) 40 mg sq q o week ________ (anakinra) 100mg sq daily ________ (infliximab) 3 mg/kg, max 1000mg q 8 weeks IV |
*Enbrel*
Humira Kineret (not used anymore) Remicade |
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Biologics: Most recently approved by FDA, usually require failure of all or most DMARD, and all or most Anti Cytokine Therapies.
_________(abatacept) dose dependent on weight, generally 750mg once monthly ________ (rituximab) B cell depleting agent given twice yearly by IV |
Orencia
Rituxan |
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More than 20 persistently inflamed joints
A rapidly declining functional capacity Elevated levels of ESR or C-reactive protein Anemia of chronic disease Hypoalbuminemia Positive rheumatoid factor tests (often in high titer) or presence in serum of anti-cyclic citrullinated peptide (anti-CCP) antibodies Extraarticular disease Evidence of inflammation on plain film radiography such as findings of osteopenia and periarticular swelling; erosions may be present. Treatment: Depends on prior failed meds. |
EARLY, SEVERELY ACTIVE RA
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Between 6 and 20 inflamed joints
Absence of extraarticular disease (most commonly) Elevated erythrocyte sedimentation rate (ESR) or serum C-reactive protein (CPR) concentration Positive rheumatoid factor or presence in serum of anti-cyclic citrullinated peptide (anti-CCP) antibodies Evidence of inflammation on plain film radiography such as findings of osteopenia and periarticular swelling; no erosions are observed. However, a more sensitive modality, such as ultrasonography or magnetic resonance imaging (MRI), may detect erosions of bone or cartilage destruction. This constellation of findings places a patient at greater risk of developing joint damage and disability . Patients presenting with moderately active, previously untreated (or only administered NSAID) disease should receive DMARD therapy in addition to an NSAID Treatment: One or more DMARD with start, then taper down of steroid. Move to anti-TNF if doesn’t respond within 6 months. Watch ESR, Xrays closely |
EARLY, MODERATELY ACTIVE RA
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Arthralgias and morning stiffness
Elevation in the erythrocyte sedimentation rate (ESR) or serum C-reactive protein (CRP) concentration At least three simultaneously inflamed joints No extraarticular disease No evidence of erosions or cartilage loss on plain radiographs No significant impairment of physical function Absence of rheumatoid factor or antibodies to cyclic citrullinated peptides is a favorable prognostic factor but a patient need not be "seronegative" to be categorized as having mild disease. Usually responds well with NSAID, and 1 DMARD (preferably MTX) TX: Watch Xrays and ESR to follow progression |
EARLY, MILDLY ACTIVE RA
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Other Considerations When Starting a DMARD and treating RA
Risk of _________: Make sure patient is PPD negative, Hep B negative, HIV negative. Educate patient that DMARD lower immunity. Flu and Pnumovax performed as appropriate Monitor _____ on MTX, ARAVA Monitor _____ on plaquenil and all anti-TNF Watch ____ and exam for SOB, MTX can cause ____________ as can RA. _________ can fall on chronic steroids, DM can be caused by steroids, etc. |
infection
LFT’s WBC CXR Pulmonary fibrosis Bone Density |
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abrupt onset of severe joint inflammation, often at night
subsides in ______days 75% in ______ joint urate crystals in synovial fluid may have hyperuricemia usually monoarticular |
acute gouty arthritis
3-10 days first MTP |
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Patients with UA ___ have incidence of acute gout of 5% per year
Overproduction associated with hyperuricosuria and therefore increase in _______ |
>9
renal stones |
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Epidemiology of Gout
Affects ___ of all men Two-fold increase in incidence from 1977-78 to 1995-96 in Rochester, MN (Arromdee E, et al. 2002) Earlier onset: with first attack in _________(Yu KH, et al. 2003) |
>1%
3rd to 5th decade, previously 4th to 6th decade |
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Why is gout more frequent?
-Higher survival from _______ -Increase in longevity (loss of estrogen in women as age…estrogen is uricosuric) -Dietary patterns -Increase in obesity -Increase use of diuretics and low-dose aspirin -Increase in CRI/dialysis and organ transplant (cyclosporine use) -Limitation of ________(especially in renal insufficient) Increase prevalence of _____(decrease in uric acid secretion) |
CHF and CAD
allopurinol HTN |
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Gout in the Elder
Equal gender distribution More _________tophi (eg. DIPs) Polyarticular presentation Harder to treat: --Increase GI toxicity from NSAIDs --Lower _____ |
upper extremity
GFR |
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Definitive dx Made only by _______________on microscopy
__________also allows quick ruling out of infection if WBC count in joint fluid is less than 40 wbc/hpf. |
arthrocentesis and crystal isolation
Aspiration |
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Indications for Allopurinol
Greater than 2 attacks a year Chronic ___________ Urate overproducer Purine enzyme defects Hyperexcretion of urate (800mg/24 hours) ___________ With cytolytic therapy for hematologic malignancies |
tophaceous gout
Nephrolithiasis |
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Diet and Gout
-_____________products lowered the risk of 1st gout attack (casein and lactalbumin uricosuric) -Seafood, red meat, anchovies, aged and smoked cheese and meats and sweetbread increase risk of attack -Beer is high in ______and leads to increase risk of attack |
Low-fat dairy
purine |
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pseudogout
pseudo - RA pseudo - OA pseudo - neurotrophic Joints Asx Chondrocalcinosis |
CPPD Crystal Deposition Dz.
Presentations |
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-hyperparathyroidism, fam. hypocalciuric hypercalcemia, hemochromatosis, hemosiderosis, hypophosphatasia, hypomagnesemia, hypothyroidism, gout, neuropathic joints, aging, amyloidosis, trauma
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CPPD Crystal Deposition Dz.
Associations |
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Wilson’s disease
Hemachromatosis/ Hypothyroidism Idiopathic Parathyroid (hyper)/ Phosphatemia (hypo) Acromegaly/amyloidosis DJD Ocranosis Gout |
Associations: Chondrocalcinosis
(WHIP A DOG) |
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Therapy for CPPD
Treat underlying association __________ NSAIDs __________ IA corticosteroids |
Colchicine
Prednisone |
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basic calcium phosphate
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milwaukee shoulder
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Take-Home Points
Gout … not just in men ___________presentation in elders Consider ____________even when history of crystalline arthropathy is present Know the indications for allopurinol Counsel your patients on appropriate diet and weight loss Remember, ___________should not be started in acute setting Know disease associations with chondrocalcinosis Know what CPPD and sodium monourate crystals should look like and the 2 can be seen concurrently Remember that colchicine causes ________in patients with decrease GFR |
Polyarticular
septic arthritis allopurinol myopathy |
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Previously thought to be a consequence of aging
hence “DJD” Now thought to be caused by joint integrity, _________, local inflammation, mechanical forces, cellular/biochemical processes |
Osteoarthritis
genetics |
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OA:
General Clinical Presentation Generally in population over age __. Symptoms: PAIN!, progressive decreased activity, as it worsens pain occurs at rest, ___________less than 30 minutes. Remember: How long is the am stiffness of RA? |
40
stiffness |
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OA
Exam findings: Tenderness to palpation No warmth, no erythema generally. Joint effusion: noninflammatory, normal viscosity, modestly elevated protein ct. __________!! (loss of smooth articulating surface). __________(Bone spurs) at the periphery of the joints |
CREPITUS
Osteophytes |
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OA generally affects _______________BUT Usually spares elbow, wrist, ankles.
Hands: Dip: ________ PIP: ________ First CMC (squared) |
fingers (PIP/DIP more than MCP), knees, hips, spine.
Heberdens Bouchard |
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Feet - 1st MTP. ________.
Knees – Minimally bone spurs, effusion, crepitus, decreased ROM. Xrays: varus (medial loss) “_________” valgus (lateral loss) “__________” Bakers Cyst: popliteal fossa ____________usually first site of cartilage loss. |
Bunions
bow legged knock knees Medial compartment |
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Hips:
Determine if in the true hip or referred from the _________. Pain in the ______ can be referred to the hip. Trochanteric bursa vs. the true hip. (pain in the groin is the key generally – no limited motion.) Limited internal/external rotation, limited flexion/extension. ALWAYS think about ____in someone with risk factors and hip pain. |
spine
knee AVN |
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OA
Spine: most common at _________ Why? Sites of most flexibility along spine. Two important syndromes associated with OA of the apophyseal joints ___________– bone spurs from the margin of the vertebral body that compromises the spinal canal. ____________– can compromise the neural foramen and impinge exiting nerve roots |
C5, T8, L3
Cervical spondylosis Uncovertebral spurs |
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____________can cause spinal stenosis, low back pain with radicular type radiation, and pseudo claudication type symptoms that respond more quickly to rest than true claudication.
___________: slipping of one vertebral body on another. |
Lumbar apophyseal osteophytes
Spondylolisthesis |
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OA Shoulders:
__________: anterior pain that worsens with time and with movement. __________: usually vague tenderness on the joint itsself. Bone spurs on the underside of the AC joint can cause rotator tendonitis/ or rotator tears. __________: aggressive/rapid deterioration of the shoulder joint secondary to calcium crystal disease. |
Glenohumeral
AC joint Milwaukee shoulder |
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What will you find on an OA xray?
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Joint space narrowing
Subchondral sclerosis Osteophytes Subchondral cysts |
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Laboratory?
Generally labs are _______with OA Acute phase reactants elevated: -When OA is associated with a crystal -Maybe at the initial onset that generally is more inflammatory than chronic disease. -When acute phase reactants remain elevated, and xrays show erosions, think ___________….treated like RA with ________,________,____ Joint fluid analysis: wbc, crystals, viscosity |
negative
inflammatory OA plaquenil, doxy, or MTX |
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OA Differential Diagnosis
____: hook osteophytes on xray at the PIPs. Aspiration of joint needed to view the crystal. __: MCP, PIP. Swelling is soft, warm, and tender. Stiffness greater than 30 min. Erosions on xray. Elevated CRP, ESR, RF, CCP Ab. _____________: Highly inflammatory fluid, one joint involved, +/- febrile, culture +. |
CPPD
RA Infectious Monoarticular arthritis |
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OA Treatment
Pain: OTC NSAIDS, Tylenol, etc. NSAIDS: ________200mg po qd (assess risk factors for stroke/MI before starting). _______7.5-15 mg po qd _______250 – 500 mg bid _______10-20mg qd |
Celebrex
Mobic Naprosyn Feldene (piroxicam) |
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Treatment
Pain – Narcotic : Darvocet, Tramadol, Lortab. Stiffness: ______1000 mg bid, paraffin baths, Physical therapy Stiffness/Pain/preventative: ________1500mg/Chondroitin 1200mg po qd Last resort or if uncontrolled superimposed crystal disease: low dose __________5-10 mg qd. |
Flaxseed Oil
Glucosamine prednisone |
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SLE Epidemiology
Prevalence: 40-50 per 100,000 1 in 2000 in the U.S. Peak incidence age ______ Female to male ratio ____:1 |
15-40
6-10 |
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Higher prevalence in:
Urban __ rural areas Asians, Asian Indians in England African-americans, afro-Caribbeans Hispanics Lower prevalence in: Blacks in ________ |
>
Africa |
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__________ have a poorer prognosis
Psychosis Proteinuria Serositis +Sm (Smith), RNP Discoid lupus ______: Higher one-year mortality More serositis Less photosensitivity |
African-americans
Men |
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________:
More severe symptoms Increase incidence of malar rash, nephritis, pericarditis, hepatosplenomegaly and hematologic abnormalities ________: Decrease incidence of malar rash, +SSA/SSB, renal or CNS involvement Increased incidence of sicca, serositis and musculoskeletal manifestations |
Children
Elderly |
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Etiology- Still unknown
Multifactorial: ________ factors Familial aggregation especially amongst 1st degree relatives Concordance in monozygotic twins 25-50% and dizygotic twins 5% _________factors _________ abnormalities Environmental factors |
Genetic
Hormonal Immune |
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Pathogenesis of Clinical Manifestations:
Autoantibodies are ___________ Immune complex deposition Complement fixation ___________ cascade triggered Th2 predominant process Complements fall and dsDNA rises with ___________ Autoantibodies Precede Clinical Onset |
pathogenic
Inflammatory disease activity |
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Not all +____ is Lupus
Found in 5% of the normal population and presence increases with _____ Found in other autoimmune disease and viral infections: Hypothyroidism Neoplasm Hepatitis B and C Other CTD (RA, SSc, inflammatory myopathy) Interstitial lung disease |
ANA
age |
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Manifestation of which autoantibody:
______ - Corresponds well with disease activity Present in GN ______ - Sicca, Photosensitivity, SCLE, Vasculitis, Late onset of dz ______ - Raynaud’s, Myositis, Sclerodactyly ______ - Thrombosis, Livedo, Valvular heart disease ______ - Psychosis, Hepatitis |
ds DNA
SSA, SSB RNP aPLA (causes miscarraiges) Ribosomal P protein |
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discoid rash
arthritis malar rash photosensitivity antinuclear antibody serositis renal disorder hematologic disorder immunologic disorder neurologic disorder oral ulcers |
SLE Classification criteria
must have 4 criteria simultaneously or serially |
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________: fixed erythema, flat or raised, sparing the nasolabial folds
________: raised patches, adherent keratotic scaling, follicular plugging, older lesion may cause scarring ____________: skin rash from sunlight ____________: nonerosive, inflammatory in 2 or more peripheral joints __________: pleuritis or pericarditis |
malar rash
discoid rash photosensitivity arthritis serositis |
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____________: persistent proteinuria or celluar casts, >0.5gm
____________: seizures or psychosis ____________: hemoylytic anemia, leukopenia or lymphopenia on 2 occasions, thrombocytopenia ____________: LE cells or Abs to ds-DNA or Sm or false positive serologic test for syphilis for at least 6 months _______________: positive |
renal disorder
neurologic disorder hematologic disorder immunologic disorder antinuclear Ab test |
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Malar
Discoid SCLE Photosensitivity Oral ulcers Scarring alopecia |
Mucocutaneous Manifestations
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90% non-erosive
Deformities are reducible (Jaccoaud deformity/arthritis) |
Joint Manifestations
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Found in ~50% of SLE patients
Poor prognostic factors: African american Elevated Cr Increased proteinuria Anemia Renal biopsy with findings consistent with severe or chronic activity and crescent formation/tubulointerstitial fibrosis |
Renal*** Manifestations
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WHO Classification of Lupus Nephritis
Class 1: _____________ Class 2: ___________ disease Mild renal disease Minimally active urinary sediment +/-Active SLE serology Non-nephrotic range proteinuria |
Normal glomeruli
Mesangial |
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WHO Classification of Lupus Nephritis
Class 3: ______________ Glomerulonephritis More active urinary sediment More likely active SLE serology 25% have NRP HTN May evolve into DPGN |
Focal Proliferative
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WHO Classification of Lupus Nephritis
Class 4: _______ Most severe of renal involvement with active urinary sediment HTN Frequent NRP Reduced GFR SLE serology very active Usually on dialysis |
DPGN (diffuse proliferative glomerulonephritis)
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WHO Classification of Lupus Nephritis
Class 5: ___________ Significant NRP Less active SLE serology Bland sediment Always on dialysis |
Membranous
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Estimated to be present in 50% of patients
MRI brain may demonstrate cortical and subcortical areas of increased T2 signal enhancement Arteriogram usually normal with no true vasculitis seen at autopsy *psychosis* seizures headaches/migraines myopathy |
Neurologic Manifestations
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Pericarditis, myocarditis, endocarditis
Premature atherosclerotic disease Vasculitis Raynaud’s phenomenon |
Cardiovascular Manifestations
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Lupus pneumonitis and interstitial lung disease
Lymphocytic interstitial pneumonia Vanishing lung syndrome Pulmonary hemorrhage Pulmonary hypertension Pulmonary embolism Pleuritis Diaphragmatic weakness |
Pulmonary Manifestations
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May occur in up to 25% patients
Occurs in overlap syndrome in the presence of RNP, Raynaud’s, GERD Strictures may form induced by Esophageal candidiasis secondary to steroids Medication-induced ulcerations May present as dysmotility or dysphagia 60 to 90% SLE patients develop peritonitis during their lifetime |
Esophageal Involvement
SLE Peritonitis*** |
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Estimated to occur in 4-21% SLE patients
Secondary to NSAIDS and steroids |
Dyspepsia/PUD
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Increase risk in patients with peripheral vasculitis or CNS lupus
If perforation suspected or irreversible ischemia: NPO BC, antibiotics __________ 1-2mg/kg qd or IV _______________1-1.5gm qd x 3 days + CTX 1 gm IV or 750 mg/meter square |
Mesenteric Vasculitis and Infarct
Prednisolone methylprednisolone |
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May be from vasculitis or thrombosis in association with antiphospholipid syndrome
_________ 1mg/kg per day |
Lupus Pancreatitis
Prednisolone |
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Cirrhosis
Cholestatic picture Chronic active or persistent hepatitis Granulomatous hepatitis Centrilobular necrosis PBC (associated with +Ro/SSA) Steatosis/fatty liver Liver toxicity secondary to medications |
Hepatic Involvement
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Occurs in young lupus female patients
Edema and hypoalbuminemia Presents with diarrhea in 50% cases Diagnosis made by assaying increase amount of indium-labeled plasma in a 4 day stool collection and confirmed by increased 24 hour stool alpha 1 antitrypsin excretion |
Protein Losing Enteropathy
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Drug-induced lupus
Two types: systemic symptoms vs. drug-induced SCLE Thought to occur in slow acetylators of aromatic amine and hydrazine compounds ____________, ____________, _____, _________ are the most frequently associated drugs with drug-induced lupus with systemic sxs (serositis, arthritis, antihistone antibodies in 90-100% and P ANCA with INH) _____ and _____ are the most frequently associated drugs triggering SCLE (no systemic sxs) |
Hydralazine, minocycline, INH, procainimide
HCTZ and CCB |
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Treatment
_______ disease: antimalarial agents, thalidomide, prednisone, intralesion CS, MMF, dapsone, azathioprine, MTX ______ disease: antimalarial agents, MTX, Arava, azathioprine, prednisone ______ disease: corticosteroids, CTX IV, MMF, azathioprine __________: CTX IV, corticosteroids ____________(autoimmune): CTX IV, corticosteroids, plasmapheresis _______ disease: CTX IV, corticosteroids |
Skin
Joint Renal Vasculitis Thrombocytopenia CNS |
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SLE Morbidity (3)
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AVN
osteoporosis cognitive dysfunction |
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Diffuse proliferative glomerulonephritis
Hypertension Male Young African-american Poor socioeconomic status Positive antiphospholipid antibodies Overall high disease activity |
Factors Heralding a Poor Prognosis
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SLE Mortality
Early death (3) Late death (3) |
Active dz: CNS, renal, CV
Active dz, tx complications (infections), premature CAD |
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**stiff in am but gets better in late afternoon**
Exclusively affects patients over age __ Incidence varies geographically (north Europe 113/100,000, southern Italy 13/100,000 Characterized by subacute or chronic onset of aching and am stiffness in the shoulders/hip girdles, neck and torso. Usually _________ Synovitis/bursitis causes discomfort/stiffness. |
Polymyalgia Rheumatica
50 symmetric |
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DDX for PMR:
RA: Considerable overlap between PMR and RA. Usually patients present with PMR then RA secondarily. _________: slow DTR, low T4, elevated TSH ___________: Persistent fever, heart murmur, + blood cultures, vegetation on the heart valves on echo __________: usually younger than age 50. Widespread musculoskeletal pain, no constitutional symptoms, normal ESR, normal exam. ___________: symmetric proximal muscle weakness, no prominent shoulder/hip pain. Elevated CPK, elevated LFT. |
Hypothyroidism
Infective endocarditis Fibromyalgia Polymyositis |
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PMR
Physical Exam Findings Decreased ROM of the _____________. Muscle tenderness is NOT a prominent feature on exam, despite the name. ________normal ________ usually between 40-100 mm/hr. Other labs are nonspecific: __________ Imaging: not beneficial |
shoulders, neck and hips
Strength Elevated ESR normocytic anemia |
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When to think about PMR?
Age over __ Bilateral aching and morning stiffness lasting _________or more, persisting at least one month, and involving at least two of the three areas: neck, shoulders, hip girdle ESR elevated to _______or more |
50
30 minutes 40 mm/hr |
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Treatment of PMR:
Generally rapidly resolves with _____________. Patient usually reports complete loss of symptoms within 2-3 days of starting ____________orally. 25-50% of patients usually relapse. Low dose steroids chronically may be needed. |
low dose steroids
10mg of prednisone |
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spondylarthropathy
Collection of diseases that share the following clinical features: ________ inflammation (spinal/SI joints) asymmetric _________ enthesitis ______ and _____ lesions eye and bowel inflammation association with or ongoing infectious disease likely positive _______ |
axial
arthritis genital and skin HLA B27 |
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Undifferentiated spondylarthropathy
Ankylosing spondylitis Psoriatic arthritis Reactive arthritis Reiters syndrome Spondylarthropathy associated with Chrons/ulcerative colitis Juvenile spondylarthropathy |
dz included in spondylarthropathies
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Clinical Manifestations of SpA
____________: acute onset, predominantly lower extremities (knees/ankles/feet), asymmetric and occurring in 2-3 joints. Sensitivity and specificity for asymmetric oligoarthritis (1-3 joints) for spondylarthropathy is 44 and 95%. ___________: inflammation around the tendon/ligament/joint capsule/fascia insertion sites on bones. New bone forms at site causing immobility. __________: inflammation of the soft tissues between the joints. Common enthesopathy site: ____________ |
Peripheral arthritis
Enthesopathy Dactylitis achilles tendon |
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Clinical Manifestations of SpA
_______________: insidious onset in the neck/back, occurring at least 3 months, morning stiffness, improved with exercise _______________: genital characteristic of Reiters. Painless. Skin lesions (_______________) start as clear vesicular lesion that progress to maculopapular. Nonspecific ____________ with negative cultures. Inflammatory eye disease: ____________ common in Reiters. ________: more severe, acute, unilateral, redness, pain, photophobia. Can cause visual impairment. _______________: Strong link between active peripheral arthritis and histologic gut inflammation |
Inflammatory spine pain
Genital/skin/mucosal lesiions keratoderma blennorrhagica urethritis conjunctivitis Iritis Inflammatory bowel mucosal lesions |
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Evidence of preceeding infection: ReA onset of sx occurs following GU infection or diarrhea (within one month of episode.
________: chlamydia ________: shigella, salmonella, campylobacter, Yersinia |
GU infection
Diarrhea |
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Common Labs in SpA:
________ helpful, but not always +, if a patient has 3 of the criteria including xray evidence of sacroilitis then HLA B27 positivity/negativity doesn’t affect dx. Test for bacterial infections ____ test, ongoing link between positivity and SpA |
HLA B27
HIV |
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Imaging in SpA
Peripheral joints: _________ at hind foot with fluffy erosions can be seen. SI joints: ___________, usually unilateral in early disease _____________ of the spine: bony outgrowths induced by an enthesopathy on the spine. Comma shaped, lower three thoracic/upper three lumbar are common sites |
enthesitis
sacroiliitis Syndesmophytes |
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Reactive Arthritis
No generally accepted criteria __________ following infection of Chlamydia, Yersinia, Shigella, Salmonella , Campylobacter. No more than ____ weeks between infection and synovitis. Asymmetric ___________ Confirmation of infection with culture/serology or + ______ |
Synovitis
6 oligoarthritis HLA B 27 |
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Reiters Syndrome
Patient had triad: ________, ____________, __________ Term ‘incomplete Reiters” when not all criteria or met, now ‘undifferentiated SpA.’ usually in males |
uveitis, urethritis, arthritis
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Patients with criteria to be diagnosed SpA but don’t fit in any specific group
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Undifferentiated SpA
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Dx: H&P, labs, imaging.
______________: insidious onset neck/back pain, morning stiffness in spine improved with exercise, onset _______ age 40. ___ more features other than spine pain must be present: alternating buttock pain, enthesitis, arthritis, dactylitis, iritis, inflammatory bowel disease, psoriasis, elevated esr/crp, HLA B27, imaging evident of spondylitis/sacroiliitis, family h/o SpA |
inflammatory spine pain
before 2 |
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Differential
___ – small joint involvment _______________- associated with untreated urethritis in the past ______________- sausage digits present |
RA
Gonococcal Arthritis Psoriatic Arthritis |
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self limiting that never recurs
remits but recurs intermittently never subsides but waxes and wanes |
Course of Reiters, ReA, and undifferentiated SpA
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Treatments
Acute inflammation: ______(celebrex, mobic, indomethacin, etc) Local intraarticular injections __________ may be of benefit if no bacterial infection is active Antibiotics for active GU infection generally __________ 100mg qd. Self limited enteric infection, no Abx needed. Non self limited enteric infection: generally use one of the __________ ___________ (sulfasalazine) used for chronic arthritis forms. Given 500 – 1000 mg po qd to bid. ____________ and/or ____: joint/spine involvement |
NSAID
Steroids doxycycline quinolones Azulfidine Anti TNF alpha agents and/or *MTX* |
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Chronic inflammation of the axial skeleton
Young adult onset age 20-30. Name refers to a fibrous or bony bridging of joints |
Ankylosing Spondylitis (AS)
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Clinical Features
__________: improves with exercise, before age 40. “wakes me up in the middle of the night.” _________: SI joint involvement Limited __________: decreased flexion forward (+Schober), increased flexion of the neck (head to wall), increased thoracic kyphosis, loss of lumbar curves. Hip pain _______ pain: inflammation of the suprspinatus tendon into greater tuberosity of humerus limits mobility. ____________: generally acute, nonerosive, nondeforming. One joint to 2-4 joints (oligo) ___________ of heel ______________: fatigue/malaise secondary to poor sleep secondary to back pain at night |
Low back pain
Buttock pain spinal mobility Shoulder Peripheral arthritis Enthesitis Constitutional Symptoms |
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Imaging:
___ joint involvement __________/osteitis at ischial tuberosities, iliac crest, pubic symphysis, femoral trochanter. *________ of vertebral bodies* Bridging ___________ Calcification of __________________ ___________ of facet joints |
SI
Erosions Squaring syndesmophytes anterior longitudinal ligament Ankylosis |
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Extra articular involvement:
_________/________– needs to be treated by opthalmologist ___________ symptoms: result of cord/spinal nerve compression caused by: fracture of ankylosed spine, atlanto-axial subluxation, cauda equina syndrome _____ disease:usually aortic regurg. Caused by scarring of the aortic valve cusps and aorta. _________ disease: restrictive chest expansion. Some with pulmonary fibrosis. ________ disease: analgesic abuse nephropathy the most common occurrence. __________ ulcerations Osteopenia |
Uveitis/Iritis
Neurologic CV Pulmonary Renal Bowel mucosa |
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Goals of Therapy:
______________— To eliminate, or reduce to the minimum level possible, symptoms such as pain and stiffness. ____________— To return the patient to the best possible functional capacity. _____________— For those patients with hip or shoulder and/or peripheral joint involvement, to prevent joint destruction or bony ankylosis. _____________— To prevent progressive bony erosions and ankylosis of the spine to maintain spinal mobility, and prevent development of spinal deformities. Minimize __________ and __________ manifestations — To reduce the impact of AS-associated disorders such as uveitis and aortic valve insufficiency Prevent complications of ___________— To prevent spinal fractures, flexion contractures especially of the cervical spine |
Symptomatic relief
Restore function Prevent joint damage Prevent spinal fusion extraspinal and extraarticular spinal disease |
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Treatments
Acute inflammation: _____(celebrex, mobic, indomethacin, etc) Local intraarticular injections _________ (sulfasalazine) used for chronic arthritis forms. Given 500 – 1000 mg po qd to bid. _________ and _____: joint/spine involvement now indicated for spine involvement |
NSAID
Azulfidine anti TNF and MTX |
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Psoriatic Arthritis
Several clinical patterns of joint involvement have been identified: Distal arthritis, characterized by involvement of the _____ joints Asymmetric oligoarthritis in which less than ___ small and/or large joints are affected in an asymmetric distribution Symmetric polyarthritis, similar and at times indistinguishable from ____ ___________, characterized by deforming and destructive arthritis Spondyloarthropathy, including both ___________ and ____________ |
DIP
5 RA Arthritis mutilans sacroiliitis and spondylitis |
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Other Rheumatic Features of PsA
___________ ___________ of the flexor tendons of the hands, the extensor carpi ulnaris, or at other sites ___________ ______ lesions — pits and onycholysis |
Enthesitis
Tenosynovitis Dactylitis Nail |
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Imaging:
coexistence of erosive changes and new bone formation in the ______ joints lysis of the terminal _________ fluffy periostitis and new bone formation at the site of _________ gross destruction of isolated joints "__________" appearance occurrence of both joint lysis and ankylosis in the same patient |
distal
phalanges enthesitis **pencil-in-cup **(classic) |
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NSAIDS
Steroids IA steroids MTX, ARAVA, Azulfidine Anti TNF (Enbrel, Humira, Remicade) all now indicated for skin disease as well |
Treatment of PsA:
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Chronic Vasculitis of large and medium vessels.
Occurs in people over age 50 (200 per 100,000) Usually involves the cranial branches of the arteries that originate from the aortic arch |
Giant Cell (temporal) Arterits
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GCA S/S:
Onset is generally _________. Systemic Symptoms: _________ Symptoms associated with narrowing/inflammation, and/or occlusion of the characteristic arteries e.g. Head Pain, Jaw claudication, visual loss, arm claudication, polymyalgias, tenosynovitis, upper respiratory symptoms, aneurysm, aortic dissection, Risk of Cancer, etc |
gradual
fever, fatigue, weight loss |
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GCA:
Head Pain: New onset headache occurs in at least 2/3 of patients. Localized over ___________. May become progressive worse, or start to remit for treatment is sought. Tender temporal/occipital arteries usually found in ____ of patients. Jaw claudication: fatigue with chewing. Tongue claudication: Tongue pain/fatigue with chewing/talking. Visual Loss: Permanent or partial loss of vision can occur. GCA is an ocular emergency!! Usually complain of __________ Arm claudication: ___________arteries become narrowed. Patient complains of numbness/paresthesia to the affected side. |
temporal arteries
1/3 abrupt partial field defect subclavian/axillary |
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GCA
-Polymyalgia: aching and am stiffness in the shoulder, hip girdle, neck. *ESR over 40*. Not usually associated with ________. 40-50 % of patients with GCA have __________. -Tenosynovitis -Upper respiratory: 10% complain of __________, sore throat. -Aneurysms: __________is a late, serious finding that requires q 3-6 month monitoring dependent on size. -Aortic dissection: Can occur with or without anuerysmal dilation. |
fever
secondary PMR cough, non productive aortic aneurysm |
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GCA Exam Findings
Usually patient presents __________. Tender or thickened ____________, maybe visually swollen and/or erythematous. Bruits heard on auscultation of the ____________areas, brachial/axillary arteries |
chronically ill
cranial arteries carotid or supraclavicular |
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GCA Laboratory
High ESR often ______ _____________anemia Microscopic hematuria (glomerular origin) Increased liver enzymes Increased factor __________ related to vascular inflammation |
>100 mm/hr
Normochromic VIII/von Willebrand factor |
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When to consider GCA?
Age over ___. Headache Abrupt loss of _______. Symptoms of PMR Unexplained __________ High ESR >100 mm/hr High CRP |
50
vision fever or anemia |
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How to Confirm the Diagnosis?
____________ by a skilled vascular surgeon. Biopsy timing: ideal to perform before treatment, however, if visual symptoms are occurring treatment may be needed before biopsy to prevent visual loss. |
Arterial Biopsy
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Treatment OF GCA
_________: Start at 60mg/day oral. Once ESR starts to normalize and symptoms remit, start decreasing prednisone slowly. ____________ agent may be needed, e.g. MTX. |
Corticosteroids
Steroid Sparing |
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calcifications along tendon insertions
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fibromyalgia
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FM:
women __ men presents w/ ________ _______ sleep & exercisors anxiety/depression --------------------- these pts research dz on internet and think this is a debilitating chronic dz. |
>
pain all over poor |
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FM dx must have 5/8:
1. ________epicondyle 2. Ant. _______ chain 3. Ant. _______ wall 4. Supraspinatus 5. Trapezius 6. Post _________ 7. _________Bursa 8. _________Bursa |
1. lat
2. cerrvical 3. chest 6. Iliac Spine 7. Trochanteric 8. Anserine |
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FM tx:
-encourage good health -___________: elavil(amitriptyline) 10-50 mg, Ambien 10 mg, Ambien CR 6.25-12mg, Lunesta 2-3 mg, Rozerum 8mg - 30 min cardio 3x/wk - ___________: cymbalta 20-60mg, effexor , lexapro 10-20mg - ________: coQ10, Provigil **AVOID PAIN MEDS & HANDICAP TAGS** |
sleep meds
Anxiety/Depression fatigue |
