RA Flashcards
RA و
ویژگی های Characteristicش رو در یک جمله شرح بده
سیر بیماری چطوره ؟
Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory dis- order that is characterized by symmetrical joint pain and swelling, morning stiffness, and fatigue.
RA has a variable disease course, often with periods of exacerbations and, less frequently, disease quiescence.
پیامد های RA چه رنجی دارن؟
اگه درمان نشه؟
Outcomes range from rarely seen remitting disease to severe disease that produces disability and, for some patients, premature death.
Without treatment, most patients have progressive joint damage and significant disability within a few years. Since the introduction of methotrexate in 1985 and tumor necrosis factor-α (TNF-α) inhibitors in the 1990s, there has been a change in the treatment paradigm; many conventional and biologic therapies are now available to effectively treat this previously debilitating chronic disease.
RA
در مرد ها شایع تره یا زن ها؟
اپیدمیولوژی سنی ش چطوره؟
خانوم ها
The disease affects individuals at any age, but most com- mon age of onset is between 50 and 60 years. RA is uncommon among men younger than 45 years of age, but the incidence rises steeply with increasing age.
چه فاکتور هایی در بیمار RA نشان دهنده poor prognosis اند؟
Poor prognostic factors include
1-high disease activity with many joints involved,
2-increased inflammatory markers,
3-high titers of rheumatoid factor (RF) and/or cyclic citrullinated peptides (CCP) anti- bodies,
4-tobacco use,
5-and erosions on radiographs.
ریسک مورتالینی به دنبالRA در مردا بیشتره یا زنا و وجود چ کورموربیدیتی هایی این ریسک رو بالا میبرن؟ 2
The increased mortality rate is more pronounced in males 👨🏻🧔🏻☠️than in females with RA and is attributed to
1-infectious complications
2-and cardiovascular disease.
پاتوژنز RA?عامل ایجادش چیه؟
As for most autoimmune diseases, RA is thought to result from a complex interaction of genetic and environmental fac- tors. RA may consist of multiple environmental stimuli leading to a common clinical presentation. There is not a known single mechanism of initiation or perpetuation. Various environmental triggers such as smoking, obesity, silica exposure, mineral oil, and organic solvents
have been associated with the development of RA.
مهم ترین فاکتور محیطی در پانوژنز RA چیه؟ با کدوم نوع RA مرتبطه؟
Smoking has the most impact, particularly on CCP antibody–positive disease; CCP- positive disease has a more distinct presentation and epidemiology than CCP-negative disease.
در بین اون ۱۰۰ ژنی که مرتبطه با RA کدموشونه که داشتنش بیشترین استعداد ابتلا رو ایجاد میکنه؟
کدومه که مرتبطه با بیماری شدید و تظاهرات extraarticular؟
The genes with the greatest impact lie in the class II major histocompati- bility (MHC) locus, accounting for approximately 60% of the genetic risk for RA.
A specific sequence on the HLA-DR haplotype involved in antigen recognition is called the shared epitope, which is strongly associated with severe RA and extra-articular manifestations.
مکانیسم افزایش ریسک RA با مصرف سیگار چیه؟
the bacteria in periodontal and mucosal lung disease, which are increased with smoking, can promote citrul- lination of bacteria leading to antibodies against multiple different citrullinated peptides. Anti-CCP antibodies are associated with aggres- sive disease.
پروسه شروع RA از کدوم قسمت بدنه و ۳ بازوی اصلی پاتوژنز بیماری که منجر به شروع میشن چیان؟
Synovial membrane inflammation characterizes RA.
Specific processes that lead to this inflammation and cellular proliferation are
1-loss of tolerance,
2-cytokine production,
3-and autoantibody production.
چه سایتوکین هایی در پانوژنز RA دخیل اند؟ (اونایی که غالب اند) 4
Several cytokine signaling pathways are involved with the predominant cytokines
1-interleukin-1 (IL-1),
2-IL-6,
3-TNF-α,
4-and granulocyte-macrophage colony-stimulating factor (GM-CSF)
detected within the synovium and peripheral blood.
در anti ccp + RA کدوم قست اولین جاییه که درگیر میشه؟
in anti-CCP–positive disease, the initial site of inflammation may be in the periodontal mucosa and lung.
در بین سایتوکین هایی که در بروز RA نقش دارند بلاک کردن کدومشون بسترین تاثیر رو در جلوگیری از پیشرفت بیماری داره؟
TNF-α blockade therapies were initially developed for other diseases but then found to be very effective for RA.
مراحل پاتوفیزیپلوژی اغاز Synovial inflammation and proliferation؟
The process of synovial inflammation and proliferation is initi- ated by an interaction between antigen-presenting cells (APCs) and CD4+ T cells. APCs display complexes of class II MHC molecules and peptide antigens that bind to specific receptors on the T cells. Clonal expansion of T-cell subsets occurs with an appropriate second signal, or co-stimulation, delivered by the APC to the T cell. Activated TH1 and TH17 T-cell subsets predominate in synovial tissues. These cell types stimulate synovial macrophages to secrete proinflammatory cytokines such as IL-1, TNF-α, GM-CSF, and IL-6 to activate inflam- matory pathways.
نقش ایمنی هومورال در پاتوژنز RA?
۳ انتی بادی شایع در این بیماری؟
In addition to cellular and cytokine processes, the humoral immune system is also involved in the pathogenesis of RA. The autoantibodies found most frequently in patients with RA are immunoglobulin M (IgM), RF, and anti-CCP. Positive RF and anti-CCP testing is associ- ated with aggressive, erosive RA, and these autoantibodies are found in serum sometimes years before patients develop signs of RA. Although a causal link has not been confirmed, CCP antibodies, combined with genetic and environmental factors (e.g., smoking, periodontal disease),
are involved in the development of RA. It is not known yet how to prevent RA in people with high risk for developing it.
وقایع فاز induction در RA؟
چه فاکتور هایی این فاز را تشدید میکنن؟
RA pathogenesis occurs in stages. In the induction phase, the anat- omy of the synovial lining within the articular joint enables recruit- ment of inflammatory cells. Cigarette smoke, bacterial products, viral components, and other environmental stimuli may amplify this pro- cess and promote a dysregulated immune system. A genetic propensity for autoreactivity may initiate a then irreversible pathway to RA.
وقایع
The destructive phase, which can be antigen dependent or indepen- dent, involves mesenchymal elements such as fibroblasts and synoviocytes.
Bone erosions result from local differentiation and activation of osteoclasts,
whereas cartilage damage appears to be caused by pro- teolytic enzymes produced by synoviocytes, macrophages, and syno- vial fluid neutrophils.
Counter-regulatory mechanisms (e.g., soluble TNF-α receptors, suppressive cytokines through regulatory T cells, protease inhibitors, natural cytokine antagonists) are not produced in high enough levels, leading to a loss of tolerance.
What is pannus?
Pannus is an abnormal layer of fibrovascular tissue or granulation tissue. Common sites for pannus formation include over the cornea, over a joint surface (as seen in rheumatoid arthritis), or on a prosthetic heart valve. Pannus may grow in a tumor-like fashion, as in joints where it may erode articular cartilage and bone. In common usage, the term pannus is often used to refer to a panniculus (a hanging flap of tissue).
شامل سلول های سینووویت فعال شده، موننوکلئار سل و T cells
پاتوفیزیولوژی اسیب مفصلی در RA?
Joint damage in RA results from proliferation of the synovial inti- mal layer forming a pannus that overgrows, invades, and destroys adjacent cartilage and bone . Fibroblast-like synoviocytes and macrophages are the predominant cellular components of the invading pannus of the synovium. Extracellular matrix damage result- ing from synovial expansion is caused by several families of enzymes, including serine proteases, cathepsins, and matrix metalloproteinases.
What are the clinical characteristics of RA? 8
1-Morning stiffness or gelling
2-Symmetrical joint swelling
3-Predilection for wrists and proximal interphalangeal, metacarpophalangeal,
and metatarsophalangeal joints
4-Erosions of bone and cartilage
5-Joint subluxation and ulnar deviation
6-Inflammatory joint fluid
7-Carpal tunnel syndrome
8-Baker cyst
یک RT تیپیکال چه ویزگی هایی دارد؟
RA manifests with a symmetrical polyarthritis that typically starts with the small joints of the hands and feet and can progress to the synovium of the wrists, elbows, shoulders, knees, and ankles.
Patients have an insidious onset of inflammatory symptoms, which are fatigue, pain, and stiffness that is worse with inactivity and is improved with movement.
Prolonged morning stiffness, usually lasting more than 1 hour, is a classic feature of RA.
چه درمان های خانگی رو ب بیمار RA میتونیم توصیه کنیم برای Morning stiffnessش؟
Often, warm water and heat will also relieve this stiffness.
۵ ویژگی ظاهری مفاصلی که در RA درگیر میشن؟
Involved joints are swollen, warm, and tender, and they may have effusions. The synovium, which is normally a few cell layers thick, becomes palpable on examination (i.e., synovitis).
چه زمانی دفورمیتی های مفصلی ایجاد میشه؟
در صورت عدم درمان
پیامد های tenosynovitis?
Tenosynovitis (i.e., inflammation of tendon sheaths) leads to tendon malalignment, stretching or shortening and exacerbates joint subluxation.
What are common joint deformities in arthritis rheumatoid?
Joint deformities leading to functional disability occur in RA after long-standing joint disease. Common deformities are ulnar deviation at the metacarpophalangeal joints and volar subluxation at those joints and at the wrists. Flexion and extension contractures in the proximal and distal interphalangeal (PIP and DIP) joints of the fingers lead to the characteristic swan-neck deformity (i.e., flexion contracture at the DIP joint and hyperextension at the PIP joint) or boutonnière deformity (i.e., flexion contracture at the PIP and hyperextension at the DIP joint).
پانوفیریولوژی کارپال تونل سندرم در RA?
Synovitis at the wrists can lead to median nerve compression and carpal tunnel syndrome. Carpal tunnel syndrome can often be the first sign of RA.
دفورمیتی های RA چه زمانیی میتونن کشنده باشن؟
Rarely, long-standing cervical spine disease may lead to C1-C2 subluxation and life-threatening spinal cord compression.
پانوفیزیولوژی تشکیل کیست baker?
Ddx? ۲
Rupture of synovial fluid from the knee into the calf (i.e., Baker cyst) may mimic deep vein thrombosis or imitate cellulitis.
What are the extra articular features of RA? 5
1-Rheumatoid nodules: subcutaneous, pulmonary, sclera
2-Interstitial lung disease
3-Vasculitis, especially skin and peripheral nerves
3-Pleuropericarditis
4-Scleritis and episcleritis Leg ulcers
5-Felty syndrome
What are the constitutional symptoms of RA?
چه زمانی ظاهر میشه
Constitutional symptoms are common with disease onset and flares; these symptoms include fatigue, low-grade fever, weight loss, and myal- gia.
اپیدمیولوژی علایم خارج مفصلی RA?
Extra-articular manifestations are more common in RF-positive patients and some epidemiologic studies have shown a decrease in extra-articular manifestations associated with newer treatments and improved disease control.
شایع ترین تظاهر خارج مفصلی RA?
ویژگی هاش؟
اپیدمیولوژی؟
The most common extra-articular manifestation of RA is rheumatoid nodules, which can occur in 30% to 40% of patients.
1-These are grossly palpable nodules
2-on the skin at pressure points along extensor surfaces, especially at the elbows.
3-Rheumatoid nodules are associated with RF positivity and tobacco use.
ندول های روماتوئید به جز سطوح اکستنسور در چه جاهای دیگه ای از بدن هستن؟
can also occur in the lungs, pleura, pericardium, sclerae, and other sites, including the heart in rare cases.
درگیری چشم در RA چه علایمی میده؟
In the eyes, RA commonly is associated with keratoconjunctivitis sicca with coexistent Sjögren’s syndrome and less often with scleritis and episcleritis.
