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115 Cards in this Set
- Front
- Back
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What is rheumatology
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study of arthritis and allied conditions including connective tissue disease and other inflammatory, degenerative, and metabolic disorders of the musculoskeletal system.
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What are the 3 types of joints
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Synarthroidal(fibrous), cartilaginous(amphiarthrosis), and synovial(diarthroidal)
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What are synarthroidal (fibrous) joints?
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little or no movement (ie skull bones)
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What are cartilaginous (amphiarthrosis) joints?
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bones made by cartilage (ie intervertebral disk)
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What are synovial (diarthroidal)
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freely movable joint - most frequently affected by rheumatoid diseases.
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The joint capsule of the synovial joint is lined by
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synovial tissue (synovium)
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The synovial tissue does not cover ____
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articulating cartilage
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What innervates the synovial tissue (synovium)
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autonomic fibers to vessels
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Are their pain fibers in the synovium
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No
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Is there blood supply to the synovium
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Good blood supply
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What are the two layers of the synovium
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subintimal and initimal
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What does the subintimal of the synovium contain?
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vascular, mast cells, and macrophages
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What is the intimal portion of the synovium?
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A cells - remove bacteria
B cells - secrete hyaluronic acid |
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What is synovial fluid and what produces it?
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synovial fluid is superfiltrated plasma and is produced by the synovium
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What are the characteristics/functions of the synovial fluid?
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clear, straw colored. thick viscosity (due to hyalrunic acid), lubricates, source of nutriens for articulating cartilage, WBC < 200 cells/mm3
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What is the mucin clot test
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Acetic acid is added to the synovial fluid. Precipitate forms with hyalrunic acid. The more precipitate the healthier the fluid.
Color of fluid becomes cloudier with increase of inflammation due to WBC. |
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What is articular cartilage?
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layer of hyaline cartilage that covers and protects the ends of each bone, reduces friction in joints and distributes forces
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What are chondrocytes
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Cartilage is not static, undergoes turnover, this degradation and formation is maintained by chondrocytes (cartilage cells).
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What is cartilage composed of?
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chondrocytes (cartilage cells), collagen, proteoglycans, protein, and water.
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Why does cartilage wear down?
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No blood supply in an adult, body changes occur with aging as in osteoarthritis.
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What occurs as cartilage wears down?
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Joint inflammation, increases synovial fluid, vascular phase of inflammation takes place in synovium (rheumatoid arthritis)
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What is Systemic Lupus Erythematosus (SLE)?
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damage of connective tissues of lungs, kidneys, and blood vessels.
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What is the precipitation of urate crystals?
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gout
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In the pathogenesis of joint inflammation; exudative _____ predominates followed by _____.
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inflammation ; degeneration ; this can result in extensive formation of granulation tissue that may become fibrous, limiting movement.
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Non-inflammatory joint disease is different from inflammatory for the following reasons:
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reduced or absent synovial membrane inflammation, lack of systemic signs and symptoms, near normal synovial fluid
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What is the most prevalent non-inflammatory join disease?
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Osteoarthritis
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What is Osteoarthritis?
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degeneration and loss of articulating cartilage in synovial joints.
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What increases the prevalence of Osteoarthritis?
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Increases in age and weight, tends to occur after age 40, in women more than men
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What is primary osteoarthritis?
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Idiopathic - not associated with known risk factors, most common, aging is the most important associated factor.
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What is secondary osteoarthritis?
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Associated with risk factors such as joint stress and trauma: only involved joints subjected to risk factors.
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What id Degeneration Joint Disease?
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Primarily a loss of articulating cartilage (becomes yellowish-grey). More water accumulates and less proteoglycans.
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What is the early stage of DJD
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cartilage loses glistening appearance.
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As DJD progresses, what occurs?
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Surfaces start to flake off, decrease in synthesis and increase in collagen breakdown. Eventually the bone is left unprotected.
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What occurs to the bone as DJD progresses?
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Bone becomes sclerotic (dense and hard) and cysts may develop in bone (synovial fluid leaks into bone), osteophytes (bone spurs) can grow out of the bone
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What breaks down the articulating cartilage as DJD progresses?
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Enzymatic processes break down articulating cartilage, cytokines (IL-1 and TNF) release proteases that are destructive, thus chondrocytes are less able to produce new collagen and proteoglycans.
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When does DJD begin to appear?
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50-60 years old, changes occur in 40s but asymptomatic
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What are the first signs of DJD
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Pain in one or more joints is the first symptom, stiffness, enlargement, range of motion.
Stiffness usually lasts 15 to 30 minutes then lessens with use. |
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How is DJD diagnosed?
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Based off of clinical and radiological findings - based on exclusion. Cystic bone changes, osteophytes, and sclerosis.
Synovial fluid usually not inflammed, may have some synovitis but usually not inflammation of joint. |
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What type of feedback system is the pathophysiology of osteoarthritis.
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Positive feedback
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What is the second most common form of arthritis?
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Rheumatoid arthritis
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What is rheumatoid arthritis?
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A chronic systemic autoimmune disease
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Rheumatoid arthritis is a _____ in which _____ is a major manisfestation
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Rheumatoid arthritis is a heterogeneous group of disorders in which inflammation of multiple joints is a major manisfestation.
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What characterizes rheumatoid arthritis?
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Fibrinoid necrosis of collagen, joint deformities, and disabilities.
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What is the onset of rheumatoid arthritis?
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Either acue or insidious
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How can rheumatoid arthritis go into remission?
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spontaneously or in response to treatment
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What are some possible sources of rheumatoid arthritis formation?
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Epstein-Barr virus, Parvovirus infection, bacteria and mycoplasms
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Etiology of rheumatoid arthritis
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No single agent responsible, combination of genetics and environment. Different stimuli for different individuals, appears an immune response is initiated by an antigen.
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What are rheumatoid factors?
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Transformed autoantibodies (IgG, IgA, IgM) that react with fragments of normal antibodies.
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Where do RF factors bind and form complexes? What type of injury is this?
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The blood and synovial membrane Type III
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What are the two distinguishable aspects of synovitis
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synovial fluid and synovial membrane
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What is the synovial fluid phase comprised predominantly of?
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PMN - they phagocytize immune complexes and release many mediators. RF in constant supply, unlike many other microorganisms.
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What is a pannus?
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Granulation tissue that covers articulating cartilage after synovial membrane inflammation
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Synovial membrane phase of synovitis
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perivascular infiltration with mononuclear cells and a striking accumulation of new blood vessels (angiogenesis)
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What is the synovial membrane rich in?
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Inflammatory cells that secrete enzymes and various other inflammatory mediators that destroy cartilage and bone, this eventually leads to joint instability and muscle atrophy.
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How do monocytes/macrophages and fibroblasts aid in destruction of articulating structures?
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Release proteases and chemotactic factors to reabsorb bone.
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What released from mast cells may also play a role in bone resorption.
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heparin
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How do immune complexes amplify the immune response?
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lead to proliferative synovitis, serves as a chemotaxic force.
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What are the constitutional symptoms of rheumatoid disease?
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fatigue, anorexia, fever, weight loss
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What is symmetrical polyarthritis?
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pain at rest and with motion from swelling and later from sclerosis.
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What is the major complaint of rheumatoid disease?
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Morning stiffness for more than 30 minutes.
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How can deformity occur in rheumatoid disease?
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Joints may become ankylosed, resulting in a loss of mobility due to pain from swelling (early) and fibrosis/sclerosis (later)
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What occurs to the muscles after extended joint disuse?
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Muscular atrophy
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What are the manifestations and proposed etiology of rheumatoid disease of the eye?
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Manifestations: Scleritis
Etiology: Vasculitis |
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What are the manifestations and proposed etiology of rheumatoid disease of the Lung?
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Manifestation: Pleuritis
Etiology: pleural based rheumatoid nodules, immune complexes |
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What are the manifestations and proposed etiology of rheumatoid disease of the heart?
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Manifestations: Pericarditis, valvular scarring
Etiology: Immune complexes, rheumatoid nodules |
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What are the manifestations and proposed etiology of rheumatoid disease of the blood?
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Manifestation: anemia
Etiology: Iron deficieny, suppression of erythrocytosis. |
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What are the manifestations and proposed etiology of rheumatoid disease of the kidney?
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Manifestation: GI
Etiology: Immune complex deposition |
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What are the manifestations and proposed etiology of rheumatoid disease of the heart?
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manifestation: conduction system
etiology: vasculitis leading to ischemia |
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What percentage of rheumatoid disease patients have circulating immune complexes and auto antibodies in serum?
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70% - 85%
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Is a test for RF factor a positive test for rheumatoid disease?
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No, is helpful but RF not seen in 30% of people with rheumatoid arthritis.
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How many diagnostic criteria are required for diagnosis of rheumatoid disease?
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4 of 7
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How is the synovial fluid viscosity affected by RA?
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It is lower due to more leukocytes
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What is the 3rd most frequent form of arthritis?
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Gout (about 2 million men in USA)
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What is the classical picture of acute severe arthritis of gout directly associated with?
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hyperuricemia - eventual uric acid deposits
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What are the sources of uric acid?
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food containing purine, synthesis of purine nucleotides, breakdown of nucleic acids (cell turnover)
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How is uric acid eliminated?
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Kidney and GI, freely filtered
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Where is uric acid reabsorbed?
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proximal tube
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Where is uric acid secreted?
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Distal tubule
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What is the primary classification of gout?
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95% - inherited defect in purine metabolism results in overproduction of uric acid, associated with some enzyme defect. Diagnosed mainly in men.
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What is the secondary classification of gout?
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Developed as a consequence of an acquired or associated disorder or the use of drugs, occurs in both men and women.
Also seen in people with immune deficiency. |
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Where is there an increase risk of gout for women?
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After menopause due to estrogen levels promoting the excretion of uric acid
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What is the cause of hyperuricemia?
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purine metabolism and kidney function.
Probably not due to abnormal purine absorption alone, increased production of uric acid, and/or a decreased renal clearance of uric acid. |
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What are the three enzyme defects linked to purine metabolism?
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HGPRT, PRPP synthetase, and glucose-6-phosphatase
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What is HGPRT?
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Lack of HGPRT could cause gout. Men with Lesh-Nyhan syndrome (x-linked recessive) get overproduction of uric acid.
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What is PRPP synthetase?
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x-linked disorder, overproduction of purine pathway and hence uric acid.
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What is glucose-6-phosphatase
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autosomal recessive disorder, decreased uric acid clearance, overproduction and under excretion of uric acid.
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What may contribute to 75% - 85% with gout?
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decreased uric acid clearance
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What is the normal value for men and women in uric acid in plasma?
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4-6mg% in men
3-5mg% in women |
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What is the value for uric acid in plasma for men and women with gout?
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9 to 10 mg%
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What percentage of hyperuricemia patients develop gout?
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5%
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What does supersaturation of uric acid cause?
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Uric acid precipitating out (lower pH, lower temperature of synovial fluid)
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What do the uric acid crystals activate?
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Hageman factor, without PMNs problem is not as severe.
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What is the first stage of hyperuricemia?
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Asymptomatic hyperuricemia - levels 9-10mg% - no overt symptoms.
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What is the second stage of gout?
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Monarticular arthritis, attacks last from several hours to several weeks (if untreated), pain usually occurs at night, and 90% of initial attacks involve a single joint.
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What causes the second stage of gout?
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Uric acid may precipitate due to trauma, drugs, alcohol.
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How long do second stage gouty attack last and are they resolved?
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Attacks are usually self limiting, last 10-14 days and when over have complete resolution.
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What is the 3rd stage of gout?
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Intracritical gout - clinical cause is variable and some patients never even have a second attack. If untreated, attacks increases in severity and frequency and more associated with systemic symptoms.
Patient asymptomatic. |
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What is the 4th stage of gout?
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Chronic soreness and aching of affected joints - persistent stiffness, eventually leads to grotesque deformities.
Chronic inflammation results from the presence of urate crystals. |
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How long does it take for acute gout to become chronic?
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Average is 11.6 years (range is 3 to 42 years)
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What does Chronic Tophaceous Gout result in the formation of?
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Granulomas and tophi
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What are tophi?
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deposit of urate crystals surrounded by granuloma (macrophages and giant cells). Direct function of degree and duration of hyperuricemia, urate less soluble at lower temperature.
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What is the most common clinical manisfestation of gout next to arthritis?
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Renal involvement - urate or uric acid nephropathy.
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What is urate nephropathy
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It is a result of the urate salt crystals in renal interstitium and resulting inflammation.
Hypertension is most common in these patients. |
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What causes uric acid nephropathy?
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Deposition of uric acid crystals (renal stones) in collecting tubules.
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What can uric acid nephropathy result in?
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Acute renal failure.
Renal stones collecting in duct much more prevalent in the patients (1000x) |
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What accounts for 10% of the deaths in patients with gout?
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Renal failure.
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What percentage of patients with gout are overweight?
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75%
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How does alcohol affect excretion of urate?
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Decreases renal excretion of urate, increases catabolism of purine nucleotides.
Beer contains large quantities of guanosine - catabolized to uric acid. |
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What does moonshine cause?
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tubular damage
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What foods are high in purines?
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Organ meats - liver, brain, etc
sardines, anchovies |
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What is the first diagnosis of gout?
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Presence of monosodium urate crystals in leukocytes found in the synovial fluid obtained from inflamed joint (found in 85% of patients)
Urate crystals found in blood of asymptomatic patients - only suggestive |
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What is the second diagnosis of gout?
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Demonstration of urate crystals in biopsy or aspirate of tophi.
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What is the third diagnosis of gout?
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Not as specific as one and two, can use combination of the following three findings:
1) Presence of hyperuricemia 2) Response of synovitis following colchicine administration 3) History of monarticulate arthritis followed by period free of symptoms. |
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How long does the therapy for gout last?
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It is a lifetime commitment.
It requires education in order to increases compliance and to have the patient make a lifestyle change. |
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Are the drugs used for acute pain and to normalize serum uric acid the same?
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No
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