Loading presentation...

Present Remotely

Send the link below via email or IM

Copy

Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.

DeleteCancel

Make your likes visible on Facebook?

Connect your Facebook account to Prezi and let your likes appear on your timeline.
You can change this under Settings & Account at any time.

No, thanks

Rheumatoid Arthritis

No description
by

Deisy Soriano

on 9 May 2014

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Rheumatoid Arthritis

Rheumatoid Arthritis
(RA)

Pathogenesis
Immune Response
Characteristics Of Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune base.
Unknown etiology. (Product of the interaction between susceptibility genes and environmental factors).
Three pathological processes independent:
1. Chronic inflammation.
2. Hyperplasia of the synovium or pannus.
3. Osteoclastogenic activity increased.


Susceptibility Genes
HLA histocompatibility system, specifically HLA-DR4.
HLA-DR DRB1
Epistasis: Genes Interaction between Disease.
Environmental Factors
Air pollution.
Inhalation particles derived combustion products.
Various microorganisms.
Molecular mimicry.
Sex hormones in the women.
Oral contraceptives.
Dyslipidemia and obesity.
Smoking cigarette.
T Lymphocytes
CD4 memory phenotype.
Increased CCR4, CCR5, CXCR3, and CX3CR1.
Block the CD28/CD86.
Th1 producing IL-2 and IFN -y.
Th17 induced by producing IL -6 and IL-17.
IL-17.
B Lymphocytes
B Lymphocytes are increased in rheumatoid synovium.
Rheumatoid Factor (RF).
Important in antigen presentation to autoreactive T cells.
Cytokines
Tumor Necrosis Factor (TNF).
IL-1 and IL -6.
Abundantly produces IL-8/CXCL8, ENA-78/CXCL5, CXCL1 and CTAP-III/CXCL7.
Chemokines CXCL16, MCP-1/CCL2, MIP-1a/CCL3.
Pannus In Rheumatoid Arthritis
Synovial membrane has two main layers:
1. Intimate layer
2. Subintimal layer
Hyperplasia of the synovial membrane.
Subintimal layer contains inflammatory aggregates.
Phenotypic transformation of fibroblasts.
Increased substances such as matrix metalloproteinases (MMPs).
Neoangiogenesis In Rheumatoid Arthritis
There is an accelerated angiogenesis processes.
The fibroblast growth factor , transforming growth factor beta and certain matrix metalloproteinase promote neovascularization.
Tissue Inhibitor of Matrix Metalloproteinases ( TIMPs ).
Erosions In Rheumatoid Arthritis
People with RA have a greater risk of osteoporosis and fractures.
There is an imbalance between bone formation and resorption again leading to bone loss.
RANKL (Receptor activator of nuclear factor NFκB ligand) is the main inducer molecule of osteoclastogenesis.
The RANKL is induced by IL-1, IL-6, IL-11, IL-17, TNF-α.
Nicole Herrera Grau
Yeraldin Huérfano Huertas
Deisy Soriano Vanegas

4HA

RANKL is coupled to its receptor RANK.
The regulatory controls osteoclastogenesis is mediated by osteoprotegerin molecule (OPG).
The importance of RANKL in the pathogenesis of bone destruction in rheumatoid arthritis.
Clinical Manifestations
Foundations of Medicine Rheumatology, H. Velez, W. Rojas, J. Borrero, J. Restrepo. Seventh edition. Corporation for Biological Research, Medellin, Colombia, 2012.
Cellular and Molecular Immunology; A. Abbas, A. Lichtman, S. Pillai, Seventh edition, Elsevier Saunders, 2012.
Pathophysiology and Treatment Rheumatoid Arthritis, M. Garcia, M. Quesada, University of Costa Rica; Drug Information Center DIC; March 2004.
American College Of Rheumatology (http://www.rheumatology.org/default.aspx)
Classification Criteria For Rheumatoid Arthritis
Articular Component
Symmetric and inflammatory (arthralgia).
Morning stiffness.
Commitment can be monoarticular, oligoarticular (4 or less) or polyarticular.
Mainly joint involvement is in the hands and feet, however may compromise ankles, elbows, shoulders, knees and hips.
When inflammation persists no destruction of cartilage, bone, soft tissue and joint deformity.
Commitment In The Hands
There is a destruction of soft tissue.
Ligamentous strusctures are expanded.
Produce fusiform fingers by the presence of synovitis and joint effusion.
Finger keypad
Swan neck deformity
Z deformities
Commitment On Elbows And Shoulders
Pain and limited motion, both flexion and extension.
There is a revolving commitment forearm.
Presented at ulnar synovitis.
Presence of rheumatoid nodules.
Commitment On Hip
The affected is located between 5% to 15% of patients.
Chronic pain.
Synovitis and effusion.
Develop acetabular protrusion, which may be complicated by fracture of the acetabulum.
In some cases distorting commitment of the femoral head.
Pearl necklace
Commitment Knee
Edema secondary to articular synovial proliferation.
Spill no evidence of cartilage damage initially.
Usually affects both knees symmetrically.
Valgus deformity is rare (Men).
There may be external rotation of the knee.
In some cases there may be a popliteal cyst (Baker's cyst).
In advanced stages of the disease, present instability of the cruciate ligaments and collateral ligaments.
Commitment Foot
Between 85% to 90% of cases.
Commitment of the metatarsophalangeal joints.
Distension of the joint capsule, synovial chronic inflammation.
Subluxation and dislocation of the metatarsal.
Deformations such as hallux valgus, mallet toe, claw toe and hammer toe.
Often presented flat foot, by altering the posterior tibial tendon.
Commitment In Other Joints
TMJ (Temporomandibular joint), which creates limitations on the oral opening, headache, and disorders masticatory.
Cricoarytenoid joint, causing hoarseness and sometimes obstruction of the airway.
Cervical spine shows me with occipital pain, headache, neck pain and movement limitation in advanced stages.
Extraarticular Component
It has been associated with genetic risk factors , clinical and environmental as:
The male
Presence of rheumatoid factor
Antinuclear
Anti -CCP antibodies
Smoking
Cardiovascular Component
The main cause of death in rheumatoid arthritis patients is cardiovascular in 50 %.
Atheromatous plaque formation.
Blood hypertension.
Systemic inflammation.
Pulmonary Component
Interstitial lung disease , pulmonary effusion , rheumatoid nodules and airway commitment.
Dyspnea or cough.
The predisposing factors for respiratory compromise are the male gender, older age and also cigarette.
There pleuritic chest pain and dyspnea.
Asymptomatic pleural effusions.
Ocular Component
Dry eye is associated with Sjögren's syndrome.
Dry eyes also occurs as a result of age, use of anticholinergic drugs, presence of hypothyroidism or hypoandrogenism.
Episcleritis and scleritis , appearing with red eyes and severe pain.
A. Scleromalacia
B. Peripheral corneal ulcers
C. Juvenile rheumatoid arthritis

Dermatological Component
Rheumatoid nodules.
Nodulosis.
Vasculitis.
Skin ulceration.
Palpable purpura.
Dermatitis.
Toxic manifestations associated with drugs.
Hematologic Component
Normocytic normochromic anemia.
Hypochromic microcytic anemia.
Macrocytic anemia.
Pernicious anemia
Thrombocytopenia.
Thrombocytosis.
Renal Component
Amyloidosis.
Medications can have an impact nephrotoxic in these patients.
Minimal change glomerulopathy.
Glomerulonephritis.
Gastrointestinal Component
Gastrointestinal disturbances are related to:
Drug use.
Gastric ulcers associated or not with
Helicobacter pylori.
Ulcerative colitis.
Crohn's disease.

Epidemiology
1% of the world population is affected by rheumatoid arthritis.
Women are three times more likely than men.
The onset usually occurs between 40 and 50 years old, however, can occur at any age.
The incidence is about 3 new cases each year per 10.000 inhabitants of the population.
Bibliography
The points that we will discuss are:
Introduction
Epidemiology
Pathogenesis
Immune response
Features
Clinical manifestations
Introduction
Full transcript