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8/3/2019 Artritis Reumatoide Expo Uvm
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ARTRITIS REUMATOIDE
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Las enfermedades reumticas son causa
de una gran demanda en los servicios de
salud, se ha estimado que alrededor del33% de la poblacin general, en algnmomento de su vida presenta una
enfermedad reumtica.
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La AR, es una de las tres enfermedadesms frecuentes en la consulta externa deReumatologa con una prevalenciaestimada hasta del 47.1%.
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Esta enfermedad, presenta un evidenteriesgo de deterioro funcional, ya que secomprob que una dcada posterior al
inicio de los sntomas, al menos 50% delos pacientes son incapaces de mantenerun trabajo de tiempo completo.
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La etiologa de la AR permanecedesconocida. Al igual que otrasenfermedades autoinmunes, se
caracteriza por una alteracin en larespuesta inmune con presencia deinflamacin crnica y produccin de
autoanticuerpos
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En 1997 Weyand y Goronzy, propusieronun nuevo modelo hipottico para lafisiopatogenia de la AR, el cual integra
factores de riesgo genticos y lacomplejidad de las respuestas inflamatoria
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Este modelo asume que la respuestainmune del husped no est involucradaen el proceso inicial de la enfermedad,
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Primera etapa
El husped se ve expuesto a un gran nmerode antgenos secundario a dao en tejidosinovial, por mltiples causas y que en formaparalela, varios genes de la respuesta inmunecomo los del HLA, genes deinmunoglobulinas y receptores de clulas
T, tienen un impacto en el tipo de respuestaque se desarrolla contra estos antgenos.
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Segunda etapa
Se origina la respuesta autoinmune
donde las clulas del sistema inmune,
especficamente linfocitos T auto-reactivos,montan una repuesta contra stos antgenos y seorigina todo un proceso inflamatorio alrededor, conla presencia de clulas como macrfagos, clulasT, B y neutrfilos, infiltradas en la membrana
sinovial inflamada
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La produccin de anticuerpos y formacinde complejos inmunes, que a su vez
ocasionan el reclutamiento de una mayorcantidad de clulas inflamatorias y susproductos
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Rheumatoid arthritis (RA) is characterizedby chronic inflammation involvingconnective tissues throughout the body,
but particularly diarthrodial joints
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To describe adequately the multiplepathogenic mechanisms operative in therheumatoid process, it is necessary to
analyze events occurring in the synovialmembrane, synovial fluid, and articularcartilage compartments.
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Features of early synovitis in
rheumatoid arthritis
Lining cell layer hyperplasia
Hyperemia
Capillary proliferation Perivascular CD4+ lymphocyte
infiltrationB-lymphocyte infiltration
Expression of MHC class II markers
MHC, major histocompatibility complex
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Adhesion molecules detected in human rheumatoid synovial
tissue
Present in synovium
Endothelium
E-selectin
P-selectin ICAM-1
ICAM-2
PECAM
VCAM-1
3 integrins
HCAM (CD44)
Leukocytes
L-selectin
ICAM-1 ICAM-3
VLA-16
LFA-1
MAC-1
HCAM (CD44)
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Lining cells
L-selectin
ICAM-1
ICAM-3
PECAM 3 integrins
HCAM (CD44)
Fibroblasts
ICAM-1
HCAM (CD44)
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Biologic effects of synovial fluid cytokines and other factors in rheumatoid
arthritis
Adhesion moleculeexpression
IL-1 TNF-
IFN-
TGF-
Chemotaxis
IL-1
TNF-
IL-8 TGF-
MCP-1
MIP-1
RANTES
PGDF187
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Macrophageactivation
IL-1
TNF-
IFN-
Lytic enzymesecretion
IL-1 TNF-
TGF-
FGF
IL-4
IL-10
IL-8
IL-11
OSM
IL-18
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Matrix macromolecule
synthesis IL-1
TNF-
IFN-
TGF-
IGF-I
CTAP-III
IL-10
Angiogenesis
TNF- IL-8
FGF
TGF-
PGDF
IGF-1
IFN-
PD-ECGF
VEGF
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Fibrosis
IL-1 TNF-
TGF-
PGDF FGF
IL-4
IL-10 IFN-
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Biologic effects of intraarticular
oxidant molecules
Depolymerization of hyaluronate
Protein cross-linking
Generation of aggregated IgG
Activation of metalloproteinases Inactivation of protease inhibitors
Generation of noxious lipid peroxides
Generation of chemotactic prostanoids
DNA damage
Apoptosis
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Biologic effects of nitric oxide pertinent
to inflammatory arthritis
Proinflammatory
DNA damage
Respiratory chaininactivation
Vascular damage Edema formation
Stimulation of angiogenesis
Stimulation of metallo-proteinase activity
Chondrocyte apoptosis
Antiinflammatory
Inhibition of cell adhesion
Inhibition of superoxide ionproduction
Inactivation of superoxideion
Inhibition of IL-6 secretion
Suppression of T-cellproliferation
Suppression of Th1cytokine production
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Biologic activities of neurokinins
Vasodilatation
Chemotaxis of neutrophils and macrophages
Neutrophil and macrophage activation
Neutrophil and macrophage degranulation
Mast cell degranulation
Stimulation of IL-1 secretion
Increased expression of adhesion molecules
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Biologic activities of fibronectin
and its proteolytic fragments
Fibroblast chemotaxis
Macrophage chemotaxis
Neutrophil degranulation Increased expression of chondrocyte
proteases
Depression of proteoglycan synthesis
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Factors involved in cartilage damage in rheumatoid
arthritis Cartilage
Articular surface disruption
Chondrocyte apoptosis
Chondrocyte cytotoxicity
Inhibition of protein synthesis
Increased synthesis ofproteinases
Oxygen radicals and nitricoxide
Immune complexes
Decreased synthesis ofprotease inhibitors
Synovial fluid Lymphocytes
NeutrophilsActive proteases
CytokinesProinflammatorypeptides
Cytotoxic antibodies Immune complexes
Neurokinins
Coagulation cascade
Pannus
Transformed fibroblasts Macrophages
Endothelial cellsNeutrophils
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1987 American College of Rheumatology revisedcriteria for the classification of rheumatoid arthritis
(traditional format) Morning stiffness
Morning stiffness in and around the joints, lasting at least 1 hourbefore maximal improvement
Arthritis of three or more joint areas At least three joint areas simultaneously with soft tissue swelling
or joint fluid observed by a physician; the 14 possible areas are(right or left): PIP, MCP, wrist, elbow, knee, ankle, and MTP
joints
Arthritis of hand joints At least one area swollen in a wrist, MCP, or PIP joint
Symmetric arthritis Simultaneous involvement of the same joint areas on both sidesof the body (bilateral involvement of PIP, MCP, or MTPacceptable without perfect symmetry)
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Rheumatoid nodules
Subcutaneous nodules over bony prominences orextensor surfaces, or in juxtaarticular regions,observed by a physician
Serum rheumatoid factor Abnormal amount of serum rheumatoid factor by any
method for which the result has been positive in
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Extraarticular manifestations of
rheumatoid arthritis
Heart Pericarditis, premature atherosclerosis,
vasculitis, valvular and valve ring nodules
Lung Pleural effusions, interstitial lung disease,
bronchiolitis obliterans, rheumatoid nodules,vasculitis
Skin Nodules, fragility, vasculitis
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Neurologic Entrapment neuropathy, cervical myelopathy,
mononeuritis multiplex (vasculitis), peripheralneuropathy
Hematopoietic Anemia, thrombocytosis, lymphadenopathy, Felty's
syndrome
Bone Osteopenia
Eye Keratoconjunctivitis sicca, episcleritis, scleritis,
scleromalacia perforans, peripheral ulcerativekeratopathy
Kidney Amyloidosis, vasculitis
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TRATAMIENTO
Nonsteroidal Antiinflammatory Drugs
control of joint inflammation
Aspirin, although effective, requires frequent dosing in largeamounts (35 g/day) and has a high incidence of side effects
NSAID distinguishes them from opioids, nonnarcoticanalgesics, salicylates, and glucocorticoids. NSAIDs workquickly to reduce pain and inflammation, but do not affect theunderlying disease process, and do not protect againstcartilage loss, bone erosion, or soft tissue damage. Most are
organic acids that share an ability to inhibit prostaglandinsynthesis by blocking cyclooxygenase (COX) enzymes
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Corticosteroids There are no precise guidelines for prescribing corticosteroids,
but as a rule prednisone doses should not exceed 10 mg/day inmen, 7.5 mg/day in women, and less in postmenopausal women.Women who take more than 7.5 mg/ day for longer than 3
months risk bone loss and should have their bone mineraldensity measured regularly
Large intravenous doses (pulses) of methylprednisolone havebeen advocated to obtain quick relief of systemic systems of RAor control flare-ups of joint disease. Infusions of 1,000 mg ofmethylprednisolone every other day for three doses acts rapidlyand the benefits may persist, sometimes up to 3 or 4 months
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Disease-Modifying Antirheumatic Drugs
Commonly used conventional DMARDsinclude hydroxychloroquine, sulfasalazine,
methotrexate, and leflunomide. Also approvedby the FDA for RA, but less frequently used,are azathioprine, minocycline, andcyclosporine A. Information on oral and
injectable gold, D-penicillamine, andchloroquine, which are seldom prescribedanymore
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Artritis Reumatoide
Rehabilitacin
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Rehabilitacin
Proceso en el que eluso combinado ycoordinado de medidasmdicas, sociales,
educativas yvocacionales, ayudan alos individuosdiscapacitados aalcanzar los mas altosniveles funcionales y aintegrarse dentro de lasociedad
Atencin y tratamientomdico.
Medidas teraputicas
Preparacin yeducacin
Suministro de ayudastcnicas
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Sistemtico
Interdisciplinario
Multidisciplinario
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Propsitos de tratamiento de la AR
Control o remisin dela enfermedad
Disminuir el dao
articular Mantener la funcin
Mejorar la calidad de
vida
Se debe tomar encuenta:
Educacin
Aspectospsicosociales
Reposo
Medios Fsicos
Ejercicio teraputico
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Reposo
Reposo absoluto?
Sndrome de
desancondicionamiento
Complicacionesosteoarticulares
Reposo relativo
Protege las
articulaciones Periodos de reposo
corto
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Medios fsicos
Calor superficial CoHuCa
Lmpara de rayosinfrarojos
Hidroterapia
Parafina
Calor profundo
Fro Estimulacin ElctricaTranscutnea TENS
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Ejercicio teraputico
Se debe tener encuenta: Grado de inflamacin
de cada articulacin
Alteracionesbiomecnicas
El estado de losmsculos vecinos
El sistemacardiovascular
Edad
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Qu ejercicios?
Pasivos
Activos
Isomtricos
Isotnicos
Resistencia
Estiramiento
Recreativos