Artritis Reumatoide Expo Uvm

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

Artritis Reumatoide Expo Uvm

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