What is the differential diagnosis of joint pain?CONSTRUCTING A DIFFERENTIAL DIAGNOSIScauses of joint pain range from common to rare from not particularly dangerous to joint and life-threateningevaluation of a patient with joint pain calls for a detailed history and physical exam (often focusing on extra-articular findings) and occasionally the sampling of joint fluid and possibly analyzing radiologic and serologic tests

How would you frame the differential?the use of 3 pivotal questionsis a single joint or are multiple joints involved (is the joint pain articular or polyarticular) ?is the pain articular or extra-articular?are the involved joints inflamed or not?the acuity of the pain may also be important

Leading Hypothesis: OATextbook PresentationOA most commonly presents in older patients as chronic joint pain and stiffness. Pain is usuallyworse with activity and improves with rest. Knees, hips, and hands are most commonly affected. Onexamination of the joints, there is bony enlargement without significant effusions. Mild tendernessmay be present along the joint lines. There is limited range of motion. Radiographs are diagnostic.Disease HighlightsA. OA is a disease of aging, with peak prevalence in the eighth decade. However, as obesity is a riskfactor, it may be seen in much younger people with severe obesity.B. More common in women than menC. Although often referred to as wear and tear arthritis, the pathophysiology is actually quitecomplicated.D. Joint destruction manifests as a loss of cartilage with change to the underlying bone seen as bonysclerosis and osteophyte formation.E. Joint distribution1. OA is most common in the knees, hips, hands, and spine.2. Nearly any joint can be affected.3. Nonweight-bearing joints other than the hand, such as the elbow, wrist, and shoulder, are lesscommonly affected by OA. The ankle is also not a common location.F. Classic symptoms include1. Pain with activity2. Relief with rest3. Periarticular tenderness4. Occasional mildly inflammatory flares5. Gelling: Joint stiffness brought on by rest and rapidly resolving with activity.6. Late in the disease, constant pain with joint deformation and severe disability is common.G. Physical exam findings1. Generally there is bony enlargement, crepitus, and decreased range of motion without signs ofinflammation or synovial thickening.2. Kneea. Crepitusb. Tenderness on joint linec. Varus or valgus displacement of the lower leg related to asymmetric loss of the articularcartilage.3. Hipa. Marked decrease first in internal and then external rotationb. Groin pain with rotation of the hip4. Handa. Tenderness and bony enlargement of the first carpometacarpal jointb. Joint involvement in decreasing order of prevalence is DIP, PIP, MCP.c. Heberden nodes (prominent osteophytes of the DIP joints)Figure 27-3 Osteoarthritis of the hand.d. Bouchard nodes (prominent osteophytes of the PIP joints)e. Figure 27-3 shows a hand with some of the classic findings of OA.5. Spinea. Signs of spinal OA vary depending on location.b. Pain and limited range of motion are common.c. Radicular symptoms resulting from osteophyte impingement on nerve roots is seen.d. Spinal stenosis with associated symptoms (radiculopathy and pseudoclaudication) can resultfrom bony hypertrophy (see Chapter 7, Back Pain).Evidence-Based DiagnosisA. The diagnosis of OA is clinical, based on a compatible history, physical exam, and radiologicfindings.B. Because of the high prevalence of OA, the diagnosis should lead the differential in any patient withsuspicious symptoms.C. Diagnostic criteria have been established.1. Handa. Pain, aching, or stiffnessb. 3 of the following(1) Hard tissue enlargement of at least 2 of the following joints:(a) Second and third DIP joints(b) Second and third PIP joints(c) First MCP joint(2) Hard tissue enlargement of 2 or more DIP joints(3) Fewer than 3 swollen MCP joints(4) Deformity of at least 1 of the joints listed in above entries a through c.2. Hipa. Hip painb. 2 of the following:(1) ESR < 20 mm/h(2) Osteophytes on radiograph(3) Joint-space narrowing on radiograph3. Knee: There are multiple criteria, the easiest to remember isa. Knee painb. Osteophytes on radiograph, andc. 1 of the following(1) Age older than 50 years(2) Stiffness < 30 minutes(3) CrepitusD. The test characteristics for these criteria are shown in Table 27-15.Table 27-15. Test characteristics for the diagnostic criteria of OA.TreatmentA. Nonpharmacologic1. Patient education and improved social support have been shown to improve pain and improvethe efficacy of pharmacologic interventions.2. Weight loss decreases the symptoms of lower extremity OA.3. Physical and occupational therapy can help patients with functional impairment due to OA.B. Pharmacologic1. Acetaminophena. Standard initial therapy given its effectiveness and low side-effect profile.b. Equally effective to NSAIDs for mild to moderate OA.2. NSAIDs are probably more effective than acetaminophen for severe OA.3. Oral combinations of glucosamine and chondroitan sulfate probably are modestly effective insome patients and have a very favorable side-effect profile.4. Intra-articular medicationsa. Intra-articular corticosteroids are very effective for acute flares of OA.b. Hyaluronic acid given by intra-articular injection may provide a small benefit to somepatients.5. Tramadol and opioid analgesics are reasonable choices for patients with severe symptoms.C. Surgical1. Arthroscopic surgery for OA is probably ineffective.2. Hip and knee replacement can have remarkable effects on decreasing pain and improvingfunction in patients in whom conservative therapy has failed

it is important to recognize that all of the monoarticular arthritides can present in a polyarticular distribution, and classically polyarticular diseases may occasionally only affect a single joint. Thus, this organization is useful to organize your thinking but should never be used to exclude diagnoses from consideration.

gout penyakit heterogen yang diakibatkan tingginya kadar asam urat dalam darah karena adanya gangguan metabolisme asam urat , sehingga kristal monosodium urat terdeposisi dalam jaringan tubuh.Manifestasi klinis :Hiperurisemia asimtomatikArtritis gout akutGout intertitialGout kronik bertofi

Gouty attacks often occur after abrupt changes in uric acid levels. Common causes are:1. Large protein meals2. Alcohol binges3. Initiation of thiazide or loop diuretics4. Initiation of urate-lowering therapy5. Worsening kidney disease

Forms of gout1. Acute gouty arthritis is by far the most common type of gout.2. Chronic arthritis can develop in patients who have untreated hyperuricemia.3. Tophaceous gout occurs when there is macroscopic deposition of sodium urate crystals in andaround joints.4. The kidney can also be affected by gout. Sodium urate stones or a urate nephropathy candevelop in patients.

Acute, inflammatory, monoarticular arthritis is an absolute indication for arthrocentesis.

Kriteria diagnosis (ACR)terdapat kristal asam urat pada cairan sendiTerdapat kristal asam urat dari tofusTerdapat 6 dari 12 parameter ( bila 2 di atas tidak ada)Artritis akut Puncak peradangan pada hari ke 1Serangan monoartritisBengkok & nyeri MTP 1Artritis unilateral meliputi MTP 17. artritis unilateral termasuk sendi tarsalDiduga ada tofusRadiografi sendi : pembengkakan pada 1 sendiRadiografi : kista subkortikal tanpa erosi sendiBiakan cairan sendi (-) saat serangan radang

penatalaksanaanNon farmakologi : modifikasi gaya hidup, istirahatkan sendi dan kompres air dingin untuk serangan akutFarmakologi : allopurinol (fisrt line), uricosuric

TreatmentA. Therapy for gout is classified as either abortive (to treat an acute flare) or prophylactic (to preventflares and the destructive effects on the joints and kidneys).B. Abortive therapy is outlined in Table 27-3.Table 27-3. Immediate therapies for gout and their potential adverse effects.1. All of the therapies are effective, and the choice is usually made by the potential adverseeffects.2. Most frequently, patients are treated with a combination of a potent nonsteroidalantiinflammatory drug (NSAID) and colchicine.C. Prophylactic therapy1. There are 5 basic indications for prophylactic therapy:a. Frequent attacksb. Disabling attacksc. Urate nephrolithiasisd. Urate nephropathye. Tophaceous gout2. Prophylactic therapy should begin with nonpharmacologic interventions to decrease uric acidlevels and decrease the risk of gouty flares.a. Abstinence from alcohol useb. Weight lossc. Discontinuation of medications that impair urate excretion (eg, aspirin, thiazide diuretics).3. Potential prophylactic treatments are listed below.a. NSAIDsb. Colchicinec. Allopurinold. Probenecide. Sulfinpyrazonef. Febuxostatg. Uricase agents (eg, pegloticase) are in the early stage for testing as prophylactic therapies.4. Colchicine should be used during the initiation of urate-lowering therapy to prevent recurrentgouty flares.a. NSAIDs may be added if necessary.b. Colchicine is usually continued for at least the first 6 months (longer in the case of patientswith tophi) of urate-lowering therapy.5. Allopurinol is usually the first antihyperuricemic drug used, although it is relativelycontraindicated in patients with chronic kidney disease or liver disease.6. If allopurinol is ineffective, uric acid excretion should be measured. Patients with low uric acidexcretion (present in 80% of patients with gout) should be given a uricosuric agent, such asprobenecid.

Calcium Pyrophosphate Deposition Disease (CPPD)A. CPPD is a crystal-induced arthropathy that can present in multiple different ways.1. CPPD is often asymptomatic, being diagnosed as an incidental radiographic finding ofchondocalcinosis, the linear calcifications of articular cartilage.2. Pseudogout is an acute, inflammatory, usually monoarticular arthritis that can be clinicallyindistinguishable from gout, except for the presence of calcium pyrophosphate dihydratecrystals in the joint fluid.3. Pyrophosphate arthropathy is a chronic arthritis that is clinically similar to OA (sometimesreferred to pseudo OA); distinguishing between the 2 conditions may be difficult. However,pyrophosphate arthropathy may affect joints less commonly affected by OA like the wrists,MCPs, and shoulders.4. A small percentage of patients with CPPD (5%) can have a chronic, inflammatorypolyarthritis resembling RA (sometimes referred to as pseudo RA).5. Rarely, CPPD can present as pseudoneuropathic arthropathy, resembling a Charcot joint. In thispresentation there is a destructive monoarthropathy,B. There are many other similarities between pseudogout and gout.1. Both are caused by the inflammatory response to crystals in the synovial space.2. Both cause acute painful monoarticular attacks.3. Both can cause polyarticular flares.4. Flares can be induced by trauma or illness.5. Both can potentially cause destructive arthropathy.6. Incidence increases with age.

Pseudogout has been associated with a number of diseases, the most common of which are:1. Hyperparathyroidism2. Hemochromatosis3. Hypomagnesemia4. Hypophosphatasia

The following characteristics should make a clinician consider the diagnosis of CPPD:1. Acute arthritis of a large joint, especially the knees, in the absence of hyperuricemia.2. Chronic arthritis with acute flares.3. Chronic arthritis involving joints that would be atypical for OA such as the wrists,metacarpophalangeal (MCP) joints, and shoulders.

A. Treat an associated underlying disease, when present.B. Acute attacks can be managed with1. NSAIDs2. Joint aspiration with corticosteroid injection3. ColchicineC. Chronic degenerative arthritis is difficult to treat. NSAIDs are usually used.

D. Common findings in RA are:1. Symmetric arthritis of the hands2. Presence of serum RF and ACPA3. Presence of radiographic changes typical of RA on hand and wrist radiographs.4. Morning stiffness is a classic finding.a. Although many people are stiff upon awakening, those with inflammatory arthritis canexperience stiffness for an hour or more.b. Morning stiffness improves with therapy.Prolonged morning stiffness is a good clue to an inflammatory arthritis.E. The joints most commonly involved are1. Handa. Wrists, MCP, and PIP joints are most commonly affected.b. Distal interphalangeal (DIP) joints are often spared.c. Ulnar deviation of the MCPs as well as swan neck and boutonnire deformities are classicfindings.Figure 27-2 Rheumatoid arthritis of the hand.d. Figure 27-2 shows a hand with some of the classic findings of RA.2. Elbow3. Knee4. Ankle5. Cervical spinea. Usually presents as neck pain and stiffness.b. C1C2 instability can occur secondary to associated tenosynovitis.(1) This can produce cervical myelopathy.(2) Advisable to radiographically image the cervical spines of patients with RA prior toelective endotracheal intubation.F. Once RA is established, joint destruction begins to occur and can be seen on radiographs. Thechronic synovitis causes erosions of bone and cartilage.G. Long-standing RA can cause severe joint deformity through destruction of the joint and injury tothe periarticular structures.H. Nonarticular findings in RA1. Rheumatoid nodules, when present, are usually over extensor surfaces.2. Dry eyes are common.3. Pulmonary nodules or interstitial lung disease4. Pericardial diseasea. Asymptomatic pericardial effusion is most common.b. Restrictive pericarditis can occur.5. Anemia of inflammation (see Chapter 6) is a typical finding in RA

RAPenyakit autoimun yang menyebabkan inflamasi sistemik kronis yang manifestasi utamanya adalah poliartritis yang progresif, namun juga melibatkan seluruh organ tubuh.Onset usia 20-60Sex perempuan > laki2

diagnosisMenurut ACR / EULAR

Acr/ elar 2010

SLEA. SLE is a truly systemic autoimmune disease primarily affecting women of childbearing age.B. Various groups are more prone to disease.1. Female:male ratio is about 9:1.2. About 5% of patients reporting a first-degree relative with the disease.3. Women of color are most commonly affected.C. Almost every organ can be involved, although the joints, skin, serosa, and kidneys are mostcommonly affected.D. The pathogenesis of the disease is related to the formation of autoantibodies to a number of nuclearantigens. The ANA is the most common.E. The most common features of SLE, both at presentation and later in follow-up, are listed in Table27-7.Table 27-7. Clinical manifestations of SLE at onset and during disease.Evidence-Based DiagnosisA. The diagnosis of SLE, especially in people with mild disease, can be difficult.B. The ACR has developed criteria to standardize the diagnosis for research purposes.1. The criteria are:a. Malar

A. The diagnosis of SLE, especially in people with mild disease, can be difficult.B. The ACR has developed criteria to standardize the diagnosis for research purposes.1. The criteria are:a. Malar rashb. Discoid rashc. Photosensitivityd. Oral ulcerse. Arthritis (nonerosive arthritis)f. Serositis (pleuritis or pericarditis)g. Renal disorder (proteinuria or cellular casts)h. Neurologic disorder (headache, seizures, or psychosis without other cause)i. Hematologic disorder (hemolytic anemia or any cytopenia)j. Immunologic disorder (anti-DNA, anti-SM, or antiphospholipid antibodies)k. Positive ANA2. The diagnosis of SLE requires the presence of 4 or more of these criteria.3. Although the same reservations about using diagnostic criteria (that were developed forresearch purposes) clinically that were discussed above in the section of RA apply here, theSLE criteria are frequently used.4. The test characteristics of these criteria are given in Table 27-8. Also included in this table arethe test characteristics for the various individual criteria.Table 27-8. Test characteristics for the ACR criteria (4 or more positive criteria) and individualcriteria in the diagnosis of SLE.

5. The presence of a malar rash, or satisfaction of the ACR criteria, is highly supportive of thediagnosis of SLE.C. Autoantibodies1. Measuring autoantibodies in SLE provides important diagnostic information.2. ANA and anti-DsDNAa. ANA is the most sensitive test for SLE. It is very nonspecific.b. Anti-DsDNA is highly specific. It is also associated with the presence of lupus nephritis.c. ANA does not vary with disease activity while anti-DsDNA does.d. The predictive values of ANA and Anti-DsDNA are(1) ANA: sensitivity, 99%; specificity, 80%, LR+, 4.95; LR, 0.0.1(2) DsDNA: sensitivity, 73%; specificity, 98%; LR+. 36.5; LR, 0.28A negative ANA essentially rules out SLE. A positive anti-DsDNA essentially rules in SLE.e. Staining patterns are often reported with the ANA.(1) These patterns correlate, to some extent, with the other specific antibodies discussedbelow and their use has, to a great extent, been supplanted by these tests.(2) In general, the meanings of the staining patterns are as follows:(a) Homogeneous: Seen in SLE, RA, and drug-induced lupus(b) Peripheral: Most specific pattern for SLE(c) Speckled: Least specific pattern. Commonly seen with low titer ANAs in peoplewithout rheumatic disease(d) Nucleolar: Common in patients with scleroderma and Raynaud phenomenon.3. Other serologies are helpful because they tend to be associated with various subsets of disease.a. Anti-RNP: Associated with Raynaud phenomenon and myositisb. Anti-SSA/Ro and anti-SSB/La: Associated with Sjgren syndrome and photosensitivityc. Anti-ribosomal P: Associated with CNS manifestations of SLE4. Table 27-9 outlines a variety of serologies that may be obtained in persons in whomrheumatologic disease is suspected

D. Complement1. Complement levels are helpful in tracking the activity of SLE but are nonspecific.2. C3, C4, and CH50 levels tend to decline during episodes of lupus activity.TreatmentA. Similar to RA, the treatment of SLE is complicated and to a great extent the purview of therheumatologist.B. In general, NSAIDs, corticosteroids, and immunosuppressants are the mainstay of therapy.C. NSAIDs are generally used for symptomatic relief of inflammatory symptoms with carefulmonitoring because of their potential nephrotoxic effects.D. Corticosteroids and hydroxychloroquine are commonly used in long-term therapy and high-dosecorticosteroids are used for disease exacerbations.E. Cyclophosphamide, mycophenolate mofetil, and azathioprine are the most commonly usedimmunosuppressants in SLE. They are used most widely for the treatment of lupus nephritis.