The differences between Rheumatoid Arthritis, Gout Arthritis &

Osteoarthritis
Criteria Rheumatoid Arthritis Gout Arthritis
Purine metabolism uric acid hyperuricemiacrystallize Monosodium urate *primary: genetic disorder *secondary: renal insufficiency, lead nephropathy, starvation or dehydration, hypothyroidism, hyperparathyroidism, drugs, and chronic ethanol (especially beer and hard liquor) abuse Foods that are rich in purine: anchovies, sardines, sweetbread, kidney, liver & meat extracts

Osteoarthritis

Aetiology

-Genetic epitope of HLADR4 & IL2RA/CD25 (Juvenile Arthritis), -environmental, -hormonal oestrogen & hyperprolactinemia, -immunologic T helper 1, B cells macrophages, dendritic cells (immune response type III) -infection Mycoplasma, Epstein-Barr & Rubella

The daily stresses applied to the joints, especially the weightbearing joints (eg, ankle, knee, hip), play an important role in the development of osteoarthritis. Risk factors age, obesity, trauma, genetics, sex hormones, muscle weakness, infection, repetitive usage, crystal deposition, acromegaly, rheumatoid arthritis, alkaptonuria, hemochromatosis, thalassemia, Paget disease

Pathophysiology

External trigger (infection, trauma) autoimmune response synovial hypertrophy & chronic joint inflammation (extra articular manifestation) destruction of cartilage, bones, tendons, ligaments

Uric acid accumulates in blood/tissue crystallization of uric acids (exspecially in acidic condition) in soft & synovial tissues naked urate crystals interact with intracellular & surface receptors of local dendritic cells & macrophages danger signal to activate the innate immune system an acute gout attack is due to multiple mechanisms, including the clearance of damaged neutrophils, recoating of urate crystals, and the production of antiinflammatory cytokines

OA classified a noninflammatory arthritis evidence shown that inflammation occurs as cytokines & metalloproteinases are released into the joint involved in the excessive matrix degradation that characterizes cartilage degeneration. Synthesis of proteoglycans swelling of the cartilage effort by the chondrocytes to repair cartilage damage may last for years/decades & is characterized by hypertrophic repair of the articular cartilage proteoglycans causing the cartilage to soften & lose elasticity compromising joint surface integrity.

Diagnosis

2010 RA classification: 1. atleast 1 joint with definite clinical synovitis 2. synovitis is not better explained by other disease Score-based algorithm: -joint involvement -serologic test results -acute phase reactant test -patients self-reporting of signs/symptoms Score > 6 definitive RA

*Hyperuricemia and the classic podagra. * A definitive diagnosis of gout is based upon the identification of monosodium urate (MSU) crystals in synovial fluid or a tophus. * Hyperuricemia plasma urate level > 420 mol/L in males &360 mol/L in females. *White blood cells & ESR may be elevated due to gout in the absence of infection.

The affected will be tender to pressure right along the joint line& movement may cause a crackling sound. Blood test rule out RF, gout The typical changes seen on Xray include: joint space narrowing, subchondral sclerosis (increased bone formation around the joint), subchondral cyst formation, and osteophytes

Treatment

Non-pharmacologic rehabilitation, heat & cold therapies, orthotics & splints, exercise, occupational therapy, adaptive equipment, joint protection & energyconservation education Pharmacologic #DMARDs [Diseasemodifying antirheumatic drugs] (2 types): *Xenobiotic gold salt (aurothiomalate), hydroxychloroquine (HCQ), sulfasalazine (SSZ), methotrexate (MTX), azathioprine (AZP), cyclosporine A *Biologic agents TNFalpha, IL-1 (central pro inflammatory cytokines) #ImmunomodulatorsAnak inra (IL-1 receptor agonist), Abatacept (t-cells inhibitors), Tocilizumab (IL6 inhibitor) #NSAIDs ibuprofen, naproxen, ketoprofen, piroxicam, diclofenac # Analgesics acetaminophen, tramadol, codeine, opiates

#The initial aim of treatment is to settle the symptoms of an acute attack. Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels. Ice applied for 20 to 30 minutes several times a day decreases pain. #NSAID usual first-line treatment for gout, Improvement may be seen within 4 hours, and treatment is recommended for 12 weeks. Eg: indomethacin, ibuprofen #Colchicine alternative for NSAIDs but with GIT side effects #Steroids used for NSAID contraindicative, lead to improvement when injected into the joint. #Prophylaxis preventing further episodes of gout, including xanthine oxidase inhibitor (allopurinol &febuxostat), uricosurics (probenecid&sulfinpyrazone) (not usually commenced until 1-2 weeks after an acute attack has resolved.

The goals of osteoarthritis treatment include pain alleviation & the improvement of functional status. Several treatment options are available for slowing/ stopping the progression of this common disorder. #Nonpharmacologic: Patient education Temperature-based modalities Weight loss Exercise Physical&Occupational therapy Unloading in certain joints (eg, knee, hip) #Pharmacologic: Corticosteroids Sodium Hyaluronate Acetaminophen NSAIDs Muscle relaxants Glucocorticoids Arthrocentesis with corticosteroid injection can be used only for knee osteoarthritis if effusion is present. 4 g/d of acetaminophen can be administered ( preferred initial treatment) Topical anti-inflammatory medications or capsaicin can be administered only for knee osteoarthritis. Low-dose NSAIDs/nonacetylated salicylates may be indicated. Narcotic analgesic use may be indicated in cases of severe pain.

Prognosis

+40% of patients become disabled after 10 years Some experience selflimiting disease & others have chronic progressive illness. There is generally a much worse prognosis of RA among patients with positive RF results, but the absence of RF does not necessarily portend a good prognosis. Rheumatoid arthritis that remains persistently active for longer than 1 year is likely to lead to joint deformities and disability.

Gout that is treated early & properly carries an excellent prognosis if patient compliance is good. During the first 6-24 months of uricosuric/ allopurinol therapy, acute attacks of gout may occur. Acute attack of gout will usually resolve in 5 to 7 days. Prognosis for resolutions of acute attacks is excellent. Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity & painless tophi.

The prognosis of osteoarthritis depends on the joints involved & the severity of the condition. No proven disease/structuremodifying drugs for osteoarthritis are currently known medication is symptom relief. The prognosis is good for patients who have undergone joint replacement, with success rates for hip and knee arthroplasty being generally more than 90%.

The differences between physical examination of Pulmonary Tuberculosis, Pleural Effusion, Hydro pneumothorax, Bronchial Asthma & Acute Pulmonary Oedema.
Pulmonary Tuberculosis (kiri) Pleural Effusion (kanan) Hydropneumothorax (kiri) Bronchial Asthma Acute Pulmonary Oedema (kanan)

Exam

Statis: dada asimetris,kiri lebih datar dari kanan Inspection Dinamis : pergerakan dada kiri tertinggal dibanding kanan

Statis: dada asimetris, kanan lebih menonjol dari kiri, sela iga kanan melebar Dinamis: pergerakan dada kanan tertinggal dibanding kiri

Statis: dada asimetris,kiri lebih datar dari kanan Dinamis : pergerakan dada kiri tertinggal dibanding kanan

Statis: dada simetris Dinamis : pergerakan dada simetris

Statis: dada asimetris, kanan lebih menonjol dari kiri Dinamis: pergerakan dada kanan tertinggal dibanding kiri

Fremitus kiri

Palpation lebih lemah

dibanding kanan

Fremitus kanan melemah dibanding kiri

Fremitus kiri lebih lemah dibanding kanan

Fremitus kiri = kanan

Fremitus kanan melemah dibanding kiri

Percussion

Kiri sonor, kanan Kanan sonor, kiri Sedikit hipersonor Kiri sonor, redup redupdari RIC Kanan sonor, kiri redup dari RIC II pada kedua lap. di seluruh bagian dari RIC V s/d hipersonor s/d RIC IV paru paru kanan RIC VIII

Auscultation

Suara nafas bronkial pada bagian apeks paru kiri, suara tambahan ronkhi basah kasar yang nyaring pada apeks paru

Vesikuler pada paru kiri, suara nafas mulai melemah dari RIC V kemudian menghilang pada RIC VI VIII, egofoni pada tepi atas RIC V

Vesikuler pada paru kanan, vesikuler melemah di paru kiri

Inspirasi normal diikuti ekspirasi memanjang dgn nada lebih tinggi disertai dengan wheezing pada seluruh lap. paru

Vesikuler pada paru kiri,vesikuler melemah, ronkhi basah halus di paru kanan