Chapter 39

Medications Used to Treat Gout:

**1) Med: Colchicine Action & Use: Lowers deposition of uric acid & interferes with leukocyte infiltration, thus reducing inflammation; does not alter serum or urine levels of uric acid; For acute & chronic management Nursing Implications: Acute management: Administer when attack begins; dosage increased until pain is relieved or diarrhea develops Chronic management: Causes gastrointestinal upset in most patients **2) Med: Probenecid (Benemid), sulfinpyrazone (Anturane) Actions & Use: Uricosuric agent; inhibits renal reabsorption of urates & increases urinary excretion of uric acid; prevents top formation Nursing Implications: Be alert for nausea and rash Risk of uric acid deposition in kidney, patient should ingest large volumes of fluids **3) Meds: Allopurinol (Zyloprim), febuxostat (Uloric) Actions & Use: Xanthine oxidase inhibitor; interrupts breakdown of purines before uric acid is formed; inhibits xanthinoxidase because it blocks uric acid formation Nursing Implications: Monitor for side effects, including: bone marrow depression, vomiting, & abdominal pain

OSTEOARTHRITIS (OA)

AKA degenerative joint disease, is: a chronic, noninflammatory (even though inflammation may be present), progressive disorder that causes cartilage deterioration in synovial joints and vertebrae. Affects the weight-bearing joints: knees and hips joints of the distal interphalangeal (DIP) proximal interphalangeal (PIP) joints of the fingers. OA is the most common and most frequently disabling of the joint disorders; it is overdiagnosed and trivialized, and frequently over- or undertreated. The functional impact of OA on quality of life, especially for elderly patients, is often ignored. ***OA has been classified as primary (idiopathic), with no prior event or disease related to the OA, and secondary, resulting from previous joint injury or inflammatory disease. The distinction between primary and secondary OA is not always clear, but the clinical presentation and symptoms are often similar.

Age related changes with RD:

Age alone causes changes in serologic studies (e.g., ESR, ANA), making interpretation of laboratory values more difficult. Decreased vision and altered balance, may be problematic if RA in lower extremities affects locomotion. Many older adults fail to follow treatment regimen of RA due to combination of: decreased hearing visual acuity memory loss depression Due to metabolic changes in the elderly, pharmacological treatment can be difficult to manage the pain. Example: Elderly more prone to side effects of any med, including NSAIDs for pain. (Could cause bleeding)

Diagnostic tests for RD:

CT & MRI are not always cost effective and therefore aren't the first diagnostic method of choice.

Complement Levels—C3, C4

Complement component levels: done if a reduction/consumption of complement component concentration is suspected C3 constitutes 70% of the total protein in the complement system (antigen-antibody complexes) Normal Values: C3: 75 to 175 mg/dL (or 0.75 to 1.75 g/L) C4: 14 to 40 mg/dL (or 140 to 400 mg/L) Implications: Decrease may be seen in active SLE, immune complex disease (i.e., RA) Decrease indicates autoimmune activity

Major Goals for Rheumatic Diseases Maintain or improve joint mobility

Management Strategy for Rheumatic Diseases Implement exercise programs for joint motion and muscle strengthening and overall health

Major Goals for Rheumatic Diseases Maintain or improve functional status

Management Strategy for Rheumatic Diseases Make use of adaptive devices and techniques

Major Goals for Rheumatic Diseases Suppress inflammation and the autoimmune response:

Management Strategy for Rheumatic Diseases Optimize pharmacologic therapy (anti-inflammatory and disease-modifying agents)

Major Goals for Rheumatic Diseases Promote self-management by patient compliance with the therapeutic regimen

Management Strategy for Rheumatic Diseases Promote social support and encouragement of change-based interventions compatible with therapeutic regimen and lifestyle

Major Goals for Rheumatic Diseases Control pain

Management Strategy for Rheumatic Diseases Protect joints; ease pain with splints/orthoses, thermal modalities, relaxation techniques

Major Goals for Rheumatic Diseases Increase patient's knowledge of disease process

Management Strategy for Rheumatic Diseases Provide and reinforce patient teaching

Rheumatoid Factor (RF)

Measures RFs, antibodies directed against the Fe fragment of IgG Determines the presence of abnormal antibodies seen in connective tissue disease Normal Values: 0 to 20 U/mL Negative titer Implications: Positive titer >1:80 Present in 80% of those with RA; positive RF may also suggest SLE, MCTD Low titers can be seen in OA The higher the titer (number at right of colon), the greater the inflammation

Uric Acid

Measures level of uric acid in serum Normal Value Men, 3.4 to 7 mg/dL (202 to 416 μmol/L) Women, 2.4 to 6 mg/dL (143 to 357 μmol/L) Biologic Crystallization Point, ≥6.8 mg/dL (408 μmol/L) Implementation: Increase is seen with gout In gout, an overproduction of uric acids occurs when there is excessive cell breakdown and catabolism of nucleonic acids

C-Reactive Protein Test (CRP)

Measures the presence of abnormal glycoprotein in response to inflammatory cytokines Normal Values: <1 mg/dL (<10 mg/L) Implications: A positive reading indicates active inflammation Often is positive for RA and SLE More sensitive than ESR test

Medical and Nursing Management of OA:

No cure or slowing of disease -focus is on pain & inflammation management -preventing/limiting disability -maintaining & improving joint function -rest & joint protection -heat & cold application -weight reduction & exercise -CAM therapies (T'chi, yoga, etc) -nutritional supplements (e.g., glucosamine (maybe inconsistent)often in combination with chondroitin) Meds: -In OA, the initial analgesic therapy is: ***acetaminophen 650 mg to 1,000 mg every 6 hours, with the daily dose not to exceed 4,000 mg/day (current debate exists concerning decreasing the maximum dose of acetaminophen to 2,600 mg/day due to liver toxicity and unintentional overdosing) -If patient has GI upset from NSAIDs, supplemental treatment with a protective agent such as misoprostol (Cytotec) may be indicated -alternative to traditional NSAIDs, treatment with the cyclooxygenase (COX)-2 inhibitor celecoxib (Celebrex) may be considered in selected patients. Other meds considered: -opioids topical analgesics such as capsaicin (Capsin, Zostrix) and methyl salicylate. -Another therapeutic approach is the intra-articular injection of hyaluronic acid, referred to as viscosupplementation. Viscosupplementation thought to provide a short-term lubricant and biomechanical benefit as well as an analgesic effect by buffering synovial nerve endings directly; it may also have some anti-inflammatory effects, and it may stimulate synovial lining cells to produce hyaluronic acid.

SCLERODERMA

Scleroderma ("hard skin"), relatively rare disease & poorly understood; cause unknown. Exposure to certain environmental and occupational agents (e.g., silica dust, heavy metals, polyvinyl chloride) and drugs (e.g., bleomycin, cocaine, fenfluramine appetite suppressants), infection, and human cytomegalovirus (CMV) and other viruses have been implicated as a potential trigger. Scleroderma is classified into: localized and systemic (systemic sclerosis) with subclassifications with each. More frequent in women than men.

Antinuclear Antibody (ANA)

Serum Immunology Measures antibodies that react with a variety of nuclear antigens Usually the first step, if antibodies are present, further testing determines specific circulating antibodies to extractable nuclear antigens (anti-dsDNA, anti-RNP, anti Ro-SSA) Normal Value Screen: negative by ELISA and IFA methods If positive by IFA, specimen is titered. Titer: <1:160 Low titers are present in elderly and some healthy adults Implications: Positive test is associated with systemic rheumatic disease such as mixed connective tissue disease, SLE, RA, scleroderma, CREST syndrome, can be seen in elderly The higher the titer, the greater the inflammation Some negative ANA findings have found to have positive anti-Ro (SSA)

Clinical Manifestations and Assessment of scleroderma:

Starts insidiously with Raynaud's phenomenon and swelling in the hands. The hallmark of scleroderma is when the skin and the subcutaneous tissues become increasingly hard and rigid and cannot be pinched up from the underlying structures (fibrosis). Wrinkles and lines are obliterated. The skin is dry because sweat secretion over the involved region is suppressed. The extremities stiffen and lose mobility. Condition spreads slowly; for years, these changes may remain localized in the hands and the feet. The face appears masklike, immobile, and expressionless, and the mouth becomes rigid. The left ventricle of the heart is involved, resulting in heart failure. The esophagus hardens, interfering with swallowing. The lungs become scarred, impeding respiration. Digestive disturbances occur because of hardening (sclerosing) of the intestinal mucosa. Progressive renal failure may occur. The patient may manifest a subset of limited cutaneous symptoms referred to as the CREST syndrome Assessment focuses on the hallmark sclerotic changes in the: -skin -contractures in the fingers -color changes or ulcerations in the fingertips due to poor circulation. Assessment of systemic involvement requires a systems review with special attention to: -GI -pulmonary -renal -cardiac symptoms. Limitations in mobility and self-care activities should be assessed, along with the impact the disease has had (or will have) on body image.

degenerative (noninflammatory) rheumatic disorder classification, inflammation occurs as a secondary process.:

The resultant secondary synovitis is usually milder, is more likely to be seen in advanced disease, and represents a reactive process. The synovitis is thought to result mainly from degeneration due to mechanical irritation of two bone surfaces. As the articular cartilage becomes damaged, the matrix (noncellular component of tissue) begins to break down; the exposed cartilage changes from a slick, smooth gliding surface to a rough fibrous network of collagen fibers. This network may later be converted to bone, locking the articulating elements into position. Fixation of a joint, called "ankylosis", eliminates the friction, but at the drastic cost of immobility

Diagnostics & labs for scleroderma:

There is no one conclusive test to diagnose scleroderma, and testing depends on the possibility or extent of organ involvement. A skin biopsy is performed to identify cellular changes specific to scleroderma. Pulmonary studies show ventilation-perfusion abnormalities. Echocardiography evaluates left ventricular function and pulmonary arterial pressure, and identifies pericardial effusion (often present with cardiac involvement). Esophageal studies demonstrate reflux esophagitis (early discriminator) and dysmotility in most patients with scleroderma. Autoantibody testing, particularly ANA, is the most useful laboratory test, with a positive result common in more than 95% of patients with scleroderma and antisclerodermal antibody (anti-sci) 70. In the presence of CREST syndrome, 90% have a positive anticentromere antibody test. Other autoantibodies demonstrate an association between scleroderma and a specific clinical pattern, such as anti-topoisomerase I antibodies and lung fibrosis, or anti-RNA polymerase I/III and scleroderma renal crisis.

Clinical manifestation facts of GOUT:

Top (deposit of crystalline uric acid) are generally associated with more frequent and severe inflammatory episodes. Higher serum concentrations of uric acid are also associated with more extensive tophus formation. Tophi most commonly occur in: synovium (synovial membrane around bone) olecranon bursa (elbow) subchondral bone (bone just below cartilage) infra patellar (just below main kneecap) and Achilles tendons subcutaneous tissue on the extensor surface of the forearms and overlying joints. They have also been found in: aortic walls heart valves nasal and ear cartilage eyelids cornea sclerae Joint enlargement may cause a loss of joint motion. Uric acid deposits may cause renal stones and kidney damage.

Diagnosis of SLE:

based on a complete H&P, examination, and diagnostic tests. SLE has extreme range of clinical manifestations without classic presentation. Diagnosis is made difficult by the variable manifestations of the disease and relies on the overall clinical picture with the correlation of: -diagnostic laboratory and imaging studies, possibly including skin biopsy The presence of at least 4 of the criteria established by the ACR is required to make the diagnosis of SLE: -Cutaneous manifestations comprise four of the 11 diagnostic ACR criteria: -malaria rash -discoid rash -photosensitivity -oral ulcers When performing an assessment, it is critical to inspect skin for erythematous rashes. The nurse asks the patient about the existence of photosensitivity, fatigue, oral ulcers, or pain in joints. Additionally, systemic involvement may encompass several organ systems; therefore, the nurse must review laboratory values or findings that might suggest that the effects of inflammation are targeting organs: -ESR -CBC - anemia or thrombocytopenia -creatinine -hematuria No single laboratory test confirms SLE. Most patients with SLE have elevated serum levels of ANA, which is another ACR criterion for SLE diagnosis. A small percent of patients will test negative for ANA but will have antibodies to the nuclear antigen anti-Ro (SSA). Other diagnostic immunologic tests that support SLE diagnosis in the presence of clinical manifestations are: -C-reactive protein -anti-double-stranded DNA (anti-ds DNA) -anti-RNA -anti-Sm (Smith) -high-titer IgG antibodies. -The double-stranded DNA test, C3, and C4 indicate whether there is a genetic component that is common in 50% to 60% of patients with SLE

Clinical Manifestations and Assessment of RA:

can be categorized as: early or late disease and as: articular (joint) or extra-articular. CLASSIC SYMPTOMS: Joint pain swelling warmth erythema (redness) lack of function Palpation of the joints reveals spongy or boggy tissue. Often, fluid can be aspirated from the inflamed joint. Characteristically, the pattern of joint involvement begins in the small joints of the hands, wrists, and feet. As the disease progresses, the knees, shoulders, hips, elbows, ankles, cervical spine, and temporomandibular joints are affected. The onset of symptoms is usually acute. Symptoms are usually bilateral and symmetric. Cardinal sign of inflammatory arthritis that can appear even before pain is morning stiffness, lasting at least 30 to 45 minutes Deformities of the hands and feet are common in RA Often the PIP (proximal interphalangeal joints-finger tips) and metacarpophalangeal (MCP)-(knuckles) joints of the hands are involved initially. The deformity may be caused by misalignment resulting from swelling, progressive joint destruction, or the subluxation (partial dislocation) that occurs when one bone slips over another and eliminates the joint space. RA is a systemic disease with multiple extra-articular features: Most common are: fever weight loss fatigue anemia lymph node enlargement Raynaud's phenomenon (cold- and stress-induced vasospasm causing episodes of digital blanching or cyanosis). Rheumatoid nodules may be noted in patients with more advanced RA. These nodules are usually nontender and movable in the subcutaneous tissue. They usually appear over bony prominences, most often on extensor surfaces or pressure points such as the elbow, are varied in size, and can disappear spontaneously. Nodules occur only in people who have RF. The nodules often are associated with rapidly progressive and destructive disease. Other extra-articular features include: arteritis neuropathy scleritis pericarditis splenomegaly Sjögren's syndrome (dry eyes and dry mucous membranes).

tophi

deposits of uric acid

Secondary gout is related to a wide number of:

diseases or drugs that decrease the kidney's ability to excrete uric acid, increase the production of uric acid, or a combination of both. Conditions associated with secondary gout include: -diabetic ketoacidosis -severe dieting or starvation -metabolic syndrome Disorders such as: -multiple myeloma and leukemia result in increased production of uric acid because of a greater cell turnover and an increase in cell breakdown. -Altered renal tubular function, either as a major action or as an unintended side effect of certain pharmacologic agents (e.g., diuretics such as thiazides and furosemide), low-dose salicylates, or ethanol, can contribute to uric acid underexcretion. -excessive intake of foods high in purines (shellfish, organ meats) may result in symptoms of gout in susceptible persons.

joint effusion:

escape of fluid from the blood vessels or lymphatics into the joint space

ankylosis:

fixation or immobility of a joint

Primary gout is characterized by:

hyperuricemia caused by an overproduction of uric acid or a decreased urate excretion in the kidney. Primary gout is often caused by an inherited disorder in purine metabolism, with a 50% incidence

In the inflammatory rheumatic disorder classification, the primary process starts with

inflammation due to an altered immune function. The inflammatory reaction includes: swelling pain loss of function Degeneration then occurs as a secondary process, spreading to the articular surfaces. The cause of degeneration of the articular cartilage is poorly understood but believed to be metabolically active and therefore is more accurately called "degradation".

Rheumatic disorders affect:

joints, bones, muscles, and connective tissues. can be minor illnesses, or they can be life-threatening diseases result in obvious limitations in mobility and activities of daily living (ADLs) manifestations are pain, fatigue, insomnia, and disturbed body image Organ failure and death may be an end result for some rheumatic disorders. condition may be patient's primary health problem or a secondary diagnosis

RA-RHEUMATOID ARTHRITIS:

most common inflammatory arthritic disorder The autoimmune reaction primarily occurs in the synovial tissue. Rheumatoid factor (RF) antibodies develop in the synovium against the immunoglobulin IgG to form immune complexes. IgG transformed to a foreign protein that the body wants to destroy Phagocytosis produces enzymes within the joint. The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation Pannus has a destructive effect on the adjacent cartilage and bone. Research has found that the inflammatory chemical messenger, tumor necrosis factor (TNF), is produced by cells at the cartilage-pannus junction and may also lead to cartilage destruction. The consequences are loss of articular surfaces and joint motion. Muscle fibers also undergo degenerative changes. Tendon and ligament elasticity and contractile power are lost. Has remissions & exacerbations

arthrocentesis:

needle aspiration of synovial fluid

pannus:

proliferation of newly formed synovial tissue infiltrated with inflammatory cells

Pathophysiology of GOUT:

use the biologic value of 6.8 mg/dL or 408 μmol/L, a level of serum uric acid above the saturation point for crystal formation Asymptomatic hyperuricemia can lead to gout pathogenesis. Attacks of gout appear to be related to sudden increases or decreases of serum uric acid levels. When deposits within a joint as urate crystals, an inflammatory response occurs, and an attack of gout begins. With repeated attacks, accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the body, such as: -great toe -hands -ear (lower temperature areas) Renal urate lithiasis (kidney stones), with chronic renal disease secondary to urate deposition, may develop.

Clinical Manifestations and Assessment of Fibromyalgia:

wide range of symptoms: the most common of which are: sleep disturbances fatigue morning stiffness muscle weakness paresthesias cognitive dysfunction ("fibro fog") chronic headaches mood disturbances Patient complains of a widespread burning pain and is often unable to discriminate if pain occurs in the muscles, joints, or soft tissues. Physical exam typically reveals point tenderness at 11 or more of 18 identified sites

Clinical Manifestations and Assessment of GOUT:

-**Most common early sign: acute gouty arthritis (recurrent attacks of severe articular and periarticular inflammation) -tophi (crystalline deposits accumulating in articular tissue, osseous tissue, soft tissue, and cartilage) -gouty nephropathy (renal impairment) -uric acid urinary calculi Four stages (or phases) of gout can be identified: 1) asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, and chronic tophaceous gout. -Phase 1, asymptomatic hyperuricemia, is when the serum urate level is high, but gout manifested by arthritis or nephrolithiasis has not yet occurred. People can remain asymptomatic throughout their lifetimes. The subsequent development of gout is directly related to the duration and magnitude of the hyperuricemia. 2) Therefore, the commitment to lifelong pharmacologic treatment of hyperuricemia is deferred until there is an initial attack of gout (phase 2). -Excruciating pain and inflammation in one or more small joints. ***The metatarsophalangeal joint of the big toe is the most commonly affected joint (90% of patients) and is referred to as podagra. The tarsal area, ankle, or knee may also be affected. Less commonly, the wrists, fingers, and elbows may be affected. Causes: Trauma alcohol ingestion dieting medications surgical stress or illness may trigger the acute attack. The abrupt onset often at night, with severe pain, redness, swelling, and warmth of the affected joint. Early attacks tend to subside spontaneously over 3 to 10 days even without treatment. 3) The attack is followed by a symptom-free period (the intercritical stage or phase 3) until the next attack, which may not come for months or years. 4) However, with time, attacks tend to occur more frequently, to involve more joints, last longer, and lead to long-term sequelae (phase 4).

Medical and Nursing Management of RA:

-NSAIDS usually first choice -salicylates -COX-2 inhibitors (2nd gen NSAID): used for GI COX-2 inhibitors must be used with caution because of the associated risk of cardiovascular disease. -DMARDS -immunosuppresive agents 1) first-choice DMARDs non biologic (2) biologic agents (3) newer, small-molecule DMARDs (4) minor DMARDs. Methotrexate (Rheumatrex, Trexall) is one of the first-choice DMARDs and has become the drug of choice due to its potency and time of action (faster than all other DMARDs). Therapeutic effects or improvement may develop in 3 to 6 weeks, compared to other DMARDs, which can take 3 to 4 months to work Black box warning exists for: unexpected, severe, and sometimes fatal myelosuppression aplastic anemia GI toxicity reported with methotrexate (usually high-dose) in combination with some NSAIDs. Additionally, methotrexate is teratogenic (capable of causing birth defects), therefore a pregnancy test should be performed if a decision is made to begin treatment in a woman of childbearing age. RN ALERT!!!-Do not give live vaccines to patients on a biologic agent. Nurses need to monitor for signs of infection (e.g., fever, cough, flu-like symptoms, open sores on body). The third major group of antiarthritic drugs is the glucocorticoids (adrenal corticosteroids). These are powerful anti-inflammatory drugs used in RA especially during exacerbations ("flares") of the disease or when needing a "bridging" medication while waiting for the slower DMARDs (e.g., methotrexate) to begin taking effect. Oral glucocorticoids, such as prednisone and prednisolone, are indicated for patients with generalized symptoms. Long-term therapy can cause serious toxicity (e.g., osteoporosis, gastric ulceration, adrenal suppression, diabetes), so glucocorticoids should be limited to patients with RA who have failed to respond adequately to all other treatment options. Intra-articular injections may be employed if only one or two joints are affected and are commonly used in severe RA. Antibiotics, the tetracycline derivatives minocycline (Minocin) and doxycycline (Vibramycin), are given to improve symptoms (morning stiffness, joint pain and tenderness, and activities of daily living) in patients with RA. These antibiotics have found to decrease the action of enzymes on cartilage degradation. Usage is seen in patients who have not responded to DMARDs. Through all stages of RA, depression and sleep deprivation may require the short-term use of low-dose antidepressant medications, such as amitriptyline (Elavil), paroxetine (Paxil), or sertraline (Zoloft), to reestablish an adequate sleep pattern and to manage chronic pain.

Classifications:

-monoarticular (affecting a single joint) -polyarticular (affecting multiple joints) then to further classify it as either: -inflammatory (e.g., rheumatoid arthritis) -degenerative, noninflammatory (e.g., osteoarthritis)

Risk Factors for Osteoarthritis (OA):

1) Aging (biggest factor in OA) 2) Obesity (greater body mass index is associated with an increased risk of knee OA; the link between OA and adipose-derived leptin is being investigated) -Genetic predisposition -Joint location (joint-specific, age-related articular cartilage changes, varying joint responsiveness to cytokines) -Malalignment of joints (can lead to rapid development of OA; congenital and developmental disorders, e.g., poorly reduced intra-articular fractures, developmental dysplasia of the hip) -Trauma (can also lead to rapid development of OA; overuse or abuse of joints, as occurs in high-impact sports; previous joint damage; excessive loading or forces such as pneumatic drill operators or frequent squatting position where up to 10 times body weight may be transmitted to the knee.) -Gender (differences in incidence after age 50 may be result of postmenopausal estrogen deficiency; articular chondrocytes possess functional estrogen receptors) -Radiologic OA is more prevalent than symptomatic OA. Meaning more people have OA that is diagnosable through X-Rays, & only 1/2 will ever develop symptoms. OA of the hand, hip, and knee become more frequent with age, and more women are affected than men after age 50

Medical and Nursing Management of SLE:

Can be life-threatening Management of acute and chronic disease. The goals of treatment include: -preventing progressive loss of organ function -reducing the likelihood of acute disease -minimizing disease-related disabilities -preventing complications from therapy. NSAIDs, antimalarials, glucocorticoids, and in severe SLE cases, immunosuppressive agents (azathioprine, mycophenolate mofetil, methotrexate) are used in the management of SLE. Corticosteroids are the single most important medication available for SLE. These drugs are used topically for cutaneous manifestations, in low oral doses for minor disease activity, and in high doses for major disease activity. IV administration of corticosteroids is an alternative to traditional high-dose oral use. Corticosteroid toxicity is a major problem, and tapering of the dosage is a primary concern. Treatment of moderate to severe SLE consists of: a period of intensive immunosuppressive therapy (induction therapy) followed by a longer period of less intensive maintenance therapy. The main objective of the induction therapy is to: -stop injury -recover function -induce remission by managing immunologic activity.

RN Alert:

Certain medications, such as hydralazine (Apresoline), procainamide (Pronestyl), isoniazid (INH), chlorpromazine (Thorazine), and some antiseizure medications, can trigger an exaggerated immune response and cause a chemical- or drug-induced SLE.

scleroderma

Chronic hardening and tightening of the skin and connective tissues. Diagnostic Studies: Contrast Radiography(X-Ray-after the patient drinks a barium solution) and MRI play a role in diagnosing advancing systems affected in scleroderma

SYSTEMIC LUPUS ERYTHEMATOSUS

Chronic inflammatory autoimmune disease with variable presentations, course, and prognosis with remissions and exacerbations. More frequent in women than in men, and African Americans and Hispanics are affected more frequently than are Caucasians

Nursing Management of FM:

Chronic pain & patients may feel as if their symptoms have not been taken seriously. Pay special attention to supporting these patients & providing encouragement Goal of FM is improve physical & mental health of patients quality of life. Interventions to promote better functioning. Greater education, lower-intensity fatigue, and using aerobic/strength training exercises predictors of physical functioning. Work with patient to increase independence, avoiding complications of deconditioning, work disability, and inability to fulfill social role. Focus on patient safety: FM has found to be associated with impaired balance and falls Stretching, aerobic exercise, and strength training should be in every patient's exercise plan. Motivational interviewing (MI) is one approach that nurses can use to promote exercise The use of telephone MI to promote exercise in patients with FM associated with improvement in level of pain and physical impairment Patient support groups may help Meditation, prayer, & other spiritual practices Careful listening to descriptions of concerns & symptoms essential to help make changes necessary to improve quality of life

FIBROMYALGIA:

Chronic pain syndrome characterized by: diffuse musculoskeletal achiness stiffness fatigue and exaggerated tenderness at 18 specified tender points. Not due to tissue damage or inflammation** Affects women more than men No known cause

Clinical Manifestations and Assessment of RA cont'd:

Clinical examination of all synovial joints should be undertaken for evidence of: tenderness swelling range of movement Evidence for synovitis should be seen by a rheumatologist within 6 weeks after onset of symptoms to facilitate early diagnosis and clinical management to achieve optimal outcomes for patients Swelling of: three or more joints involvements of the MCP metatarsophalangeal joints early morning stiffness are significant manifestations of RA Presence of deformities, such as: hyperextension of PIP joints (swan neck) flexion of PIP joints (Boutonniere) ulnar deviation, in which fingers point toward the ulnar, may be noted on examination. The patient is also assessed for extra-articular changes such as: weight loss sensory changes lymph node enlargement fatigue Nursing Alert:!!!!! Patients commonly have the inability to "wring out a wash cloth," need to hold a cup with both hands, and may complain of the sensation of having a "stone in my shoe."

Medical and Nursing Management of scleroderma:

Depends on the patient's clinical manifestations. In scleroderma, treatment includes management of acute and chronic disease. -Acute conditions require interventions directed at controlling increased disease activity or exacerbations that can involve any organ system. -Chronic condition involves periodic monitoring and recognition of meaningful clinical changes requiring adjustments in therapy. Because this is a life-altering disease that has no cure, all patients should receive counseling, during which realistic individual goals may be determined. As in the other rheumatic disorders, support measures include strategies to: -decrease pain -limit disability -maintain moderate exercise -prevent joint contractures. No specific medication regimen has proved effective but along with antiarthritic drugs, various medications are used to treat organ system involvement. Calcium channel blockers & other antihypertensive agents may provide improvement in symptoms of Raynaud's phenomenon. Patients with scleroderma have problems associated with impaired skin integrity and imbalanced nutrition, less than body requirements. The patient with advanced disease may also have impaired gas exchange, decreased cardiac output, impaired swallowing, and constipation. Providing meticulous skin care and preventing the effects of Raynaud's phenomenon are major nursing challenges. Nurses teach patients to avoid the cold and to protect fingers with mittens. In addition, warm socks and properly fitting shoes are helpful in preventing ulcers. Careful, frequent inspection for early ulcers is important, and smoking cessation is critical.*******

SLE Patho:

Disturbed immune regulation that causes exaggerated production of autoantibodies and antigens. The immune abnormalities that characterize SLE occur in five phases: -susceptibility -abnormal innate and adaptive immune responses -autoantibodies immune complexes -inflammation -damage Interactions of predisposing factors (genes, female gender, and environment) result in abnormal immune responses, specifically in B cells and T cells. These responses produce pathogenic autoantibodies and immune complexes that activate complement, form in tissue, and cause inflammation. Inflammation stimulates antigens, which in turn stimulate additional antibodies. The cycle repeats and, over time, leads to irreversible organ damage. Some individuals do not progress through all phases.

Lab tests for RD:

ESR ANA Uric Acid Complement Levels—C3, C4 C-Reactive Protein Test (CRP) Rheumatoid Factor (RF)

Rheumatic disorders:

Each synovial joint has a given range of motion, and the synovial fluid within a joint has three primary functions: lubrication nutrient distribution shock absorption Inflammation is manifested in the joints as synovitis. Rheumatic disorders always involve damage to the articular cartilages. Because articular cartilages involve some degree of inflammation and degeneration, the rheumatic disorders can be classified as either: inflammatory (e.g., RA) or degenerative, noninflammatory (e.g., OA)

Medications Used in Rheumatic Diseases Disease-Modifying Antirheumatic Drugs (DMARDs)

First-Choice DMARDs (Nonbiologic) Immunosuppressives Methotrexate (Rheumatrex) Action: Immune suppression, inhibits folic acid reductase, leading to inhibition of DNA synthesis and other cellular effects Acts faster than other DMARDs Methotrexate is gold standard for RA treatment; also useful in SLE Nursing Considerations: Assess for bone marrow suppression, GI ulcerations, skin rashes, alopecia, bladder toxicity, increased infections Monitor CBC, liver enzymes, creatinine every 2 to 4 weeks Caution with NSAID use Should be on folic acid Advise patient of contraceptive measures because of teratogenicity

Focused Assessment for scleroderma:****

Focused Assessment Cutaneous Symptoms of Scleroderma Be alert for the CREST symptoms: -Calcinosis (calcium deposits in the tissues) -Raynaud's phenomenon (spasm of blood vessels in response to cold or stress) -Esophageal dysfunction (acid reflux and decrease in mobility of esophagus) -Sclerodactyly (thickening and tightening of skin on fingers and hands) -Telangiectasia (capillary dilation that forms vascular red marks on surface of skin)

Medical/Surgical Treatment of OA:

For persistent, moderate to severe OA and erosive RA, reconstructive surgery and corticosteroids are often used. Reconstructive surgery is indicated when pain cannot be relieved by conservative measures and the threat of loss of independence is eminent. Surgical procedures include: -synovectomy (excision of the synovial membrane) -arthrodesis (surgical fusion of the joint) -tenorrhaphy (suturing of a tendon) -osteotomy (to alter the distribution of weight within the joint). -Most commonly used procedure is arthroplasty, a surgical repair and replacement of the joint. Surgery is not performed during disease flares. -Tidal irrigation (lavage) of the knee involves the introduction of a large volume of saline into the joint through cannulas and then removal of this fluid. In some cases, this procedure provides pain relief for up to 6 months.

GOUT

Gout, one of the most common of the inflammatory arthritis. Metabolic disorder marked by the deposition of monosodium urate crystals within joints and other tissues. Gout is a heterogeneous group of conditions related to a genetic defect of purine metabolism that results in hyperuricemia (excessive uric acid, a purine end product). More common in males Incidence increases with: age BMI increasing serum uric acid (urate) levels laboratory population-based norm for: men is up to 7 mg/dL and women is 6 mg/dL BUT: Some people with gout have no elevated uremic acids, and some people without gout have elevated uremic acids Two types: Primary Secondary

Pathophysiology of OA

In OA, changes in articular cartilage occur first; Eventually, secondary soft tissue changes may occur. OA is characterized by erosion of the articular cartilage, combined with hypertrophy of bone at the joint margins, resulting in new bone formation known as osteophytes or bone spurs and subchondral (the bony plate that supports the articular cartilage) sclerosis. In addition, OA is characterized by a range of biochemical and morphological alterations of the synovial membrane and joint capsule. In general, a combination of cartilage degradation, bone stiffening, and reactive inflammation of the synovium occurs. Understanding of OA has been greatly expanded beyond what previously was thought of as simply "wear and tear" related to aging.

Nursing Management of GOUT:

Pain management primary concern with acute phase of an attack. Joint should be rested and application of ice, not heat, may help with reducing discomfort. Teaching self-care measures to decrease the risk of attacks (e.g., avoidance of aspirin [because doses below 2 to 3 g/day impair renal excretion of uric acid retention and higher doses are associated with high renal excretion of uric acids], trauma, stress, alcohol) and Avoid long-term complications (e.g., importance of medication compliance). PCPs may recommend patients restrict consumption of foods high in purines, especially organ meats and shellfish; others believe that limiting protein foods or avoiding trigger foods help Patients to limit alcohol intake and to avoid fad starvation diets. It is important that patients drink plenty of fluids, at least 2,000 mL daily, to lessen renal involvement and the development of urinary stones Maintenance of normal body weight should be encouraged. Dietary restriction of sodium, fat, and cholesterol can lead to a reduction in gout symptoms and decrease effects associated with coexisting metabolic syndrome. Research is limited, but first acute gout attacks may commonly precede the diagnosis of metabolic abnormalities and associated diseases.

Medical Management of Fibromyalgia:

Patient education exercise cognitive therapy along with medication Pharm: -NSAIDs -Tramadol(only opiate shown to provide some relief) -Pregabalin (Lyrica), an analgesic, anxiolytic, and anticonvulsant (a2-d receptor ligand agent), is the first to receive FDA approval for FM use. -Psychotropic meds: duloxetine, milnacipran, (fluoxetine, paroxetine -dopaminergic agents (pramipexole) -antidepressants, particularly tricyclics (also used to restore sleep patterns) -Duloxetine (Cymbalta) -Individualized programs of exercise used to decrease muscle weakness and discomfort and improve general deconditioning that occurs in affected patients

Pannus

Proliferation of newly formed synovial tissue infiltrated with inflammatory cells Pannus has a destructive effect on the adjacent cartilage and bone. Research has found that the inflammatory chemical messenger, tumor necrosis factor (TNF), is produced by cells at the cartilage-pannus junction and may also lead to cartilage destruction. The consequences are loss of articular surfaces and joint motion. Muscle fibers also undergo degenerative changes. Tendon and ligament elasticity and contractile power are lost.

Four Guiding Principles of Motivational Interviewing (Acronym RULE)

R: Reflect Resistance When the nurse argues for change and the patient is resisting and arguing against it, the nurse should "roll with the patient resistance" (i.e., the nurse acknowledges that resistance to change is expected). The patient is the primary source of arguments and solutions. The nurse should reflect resistance nonjudgmental. U: Understand The nurse expresses empathy and communicates acceptance of the patient's experience, including the patient's ambivalence about change. Be interested in the patient's own concerns, values, and motivations. L: Listen By listening to what patients say, the nurse can tell how likely they are to change. Listen for verbs in patient narrative indicating change talk, statements in relation to desire, ability, reasons, need, commitment, and taking action. E: Empower Nurses assist patients to explore how they can make a difference in their own health, emphasizing the patient's ability to choose and carry out a plan for change. Outcomes are best when patients take an active role in their own health care.

The common connective tissue diseases are:

RA systemic lupus erythematosus (SLE) scleroderma

Labs and Diagnostics of RA:

Symmetric joint inflammation & rheumatoid nodules help diagnose RA But, certain laboratory findings can contribute to a diagnosis of RA. "RF" is present in up to 70% to 80% of patients with RA, but its presence alone is not diagnostic of RA. Anticyclic citrullinated peptide (anti-CCP) is a marker that has similar sensitivity, but potentially greater specificity to RF Some laboratories are currently doing a second generation of the test called the CCP2 assay. The ESR is significantly elevated in RA. The high-sensitivity C-reactive protein is another useful test to measure inflammation and may be done with or instead of the ESR. The RBC count and complement C3 and C4 levels are decreased. Complements may be decreased as they are "used up" in some antigen-antibody reactions. Results of antinuclear antibody (ANA), the screening test for autoantibodies (antibodies that form against self), may also be positive. Arthrocentesis shows abnormal synovial fluid that is cloudy, milky, or dark yellow and contains numerous inflammatory components, such as leukocytes and complement. Synovial biopsy can detect inflammatory cells associated with RA. Radiological studies show characteristic bony erosions and narrowed joint spaces occurring later in the disease and help in diagnosing and monitoring the progression of disease.

RA plasmapheresis:

The Prosorba Column, a blood filtration device used in apheresis, has been approved by the FDA for use in treating patients with more severe and longstanding RA who have had no response to or are intolerant of DMARDs. The device, a protein A immunoadsorption column, is used in 12 weekly 2-hour apheresis treatments to bind IgG (i.e., circulating immune complex). As the patient's blood passes through the column, RF is removed. ****If the patient is on an angiotensin-converting enzyme (ACE) inhibitor, it should be discontinued prior to treatment using Prosorba Column, as the risk of serious hypotension exists with this treatment.

Nursing Interventions of sclerodoma:

The nurse teaches safe use of heat and cold application, in 15 to 20 minute intervals, usually 3 to 4 times a day. However, there is preliminary evidence to support the use of extra-depth shoes, with or without semi-rigid insoles, to relieve pain on walking and weight-bearing Patients should be taught to avoid stooping, bending, or overreaching and to rest 5 to 10 minutes when trying to complete a task. other strategies for decreasing pain such as: relaxation techniques, imagery, meditation, and distraction. Diet: anti-inflammatory diet improves serologic and symptomatic markers of inflammation. Fish oil supplements, and omega-3 or omega-6 fatty acids, can be added to the diet. Predominantly plant-based diet, avoiding excess and high-glycemic-load calories. Strong emphasis on avoidance of potentially proinflammatory foods (e.g., trans fats, refined sugars, high saturated fats, alcohol, and caffeine in excess). The majority of the diet should be derived from four areas: -whole-grain products -fresh fruits and vegetables -legumes -seeds and nuts. These sources provide several anti-inflammatory components such as fiber, isoflavones (e.g., soybeans and soy products), carotenoids, and omega-3 free fatty acids (e.g., flaxseed). Patients can be told to keep a journal to assist in monitoring ongoing diet and symptom changes and not to expect immediate results, allowing at least 12 weeks before reevaluating benefit. Consultation with a dietitian is highly recommended for understanding and meal planning suggestions. RN Alert Some medications (i.e., oral corticosteroids) used in the treatment of rheumatic diseases stimulate the appetite and, when combined with decreased activity, may lead to weight gain. Therefore, patients may need to be counseled about eating a healthy, calorie-restricted diet. -take a warm bath or shower before bedtime to relax muscles; -showering first thing in the morning may be beneficial to reduce morning stiffness -establishing a set time to sleep and a regular wake-up time -creating a quiet sleep environment with a comfortable room temperature -avoiding factors that interfere with sleep (e.g., use of alcohol and caffeine) -positioning of joints -using relaxation exercises -getting out of bed and engaging in another activity (e.g., reading) if unable to fall asleep within 20 to 30 minutes Proper body positioning is essential to minimize stress on inflamed joints and prevent deformities that limit mobility. All joints should be supported in a position of optimal function. When in bed, the patient should lie flat on a firm mattress, with feet positioned against a footboard and with only one pillow under the head because of the risk of dorsal kyphosis. A pillow should not be placed under the knees, because this promotes flexion contracture. It is best for the patient to lie prone several times daily to prevent hip flexion contracture. Care must be taken so that splinting for comfort does not restrict mobility later. Regularly removing the splint and exercising the joint through a range of motion should be done to prevent joint "freezing." Splint modification may be needed when changes occur in joint structure. Active/self-assisted exercises involve the use of overhead pulleys or wand exercises (shoulder exercises using a wand, stick, or cane). Measures to reinforce proper body posture and increase mobility include walking erect and using chairs with straight backs. When seated, the patient should rest the feet flat on the floor and the shoulders and hips against the back of the chair. For example, swollen (edematous) hands may be more limiting than deformed hands. Motivational interviewing (MI): For example, "You say you want to exercise, but it hurts. What things can you do to help ease the pain with activity?" The nurse refrains from persuading and confronting, but guides the patient toward an acceptable resolution that triggers change.

Medical Management of GOUT:

Two major phases: 1) management of acute gouty inflammation 2) long-term management to prevent flares and to control hyperuricemia Prompt intro to anti-inflammatory used to treat inflammatory episodes in gout. NSAIDS, such as indomethacin or ibuprofen, are considered agents of first choice; indomethacin or ibuprofen with colchicine as an alternative or in combination can be considered. -Colchicine (in combination with uricosuric) single-ingredient oral colchicine product, Colcrys, for the treatment of acute gout. Other agents to relieve acute gout are: corticosteroids (oral or parenteral) or adrenocorticotropic hormones (ACTH) because of their anti-inflammatory properties. Low-dose colchicine has been used for prophylaxis after resolution of attacks, but does not prevent accumulation of urate in joints and tophi. Management of hyperuricemia, tophi, joint destruction, and renal disorders is usually initiated after the acute inflammatory process has subsided. When reduction of the serum urate level is indicated, uricosuric agents are the medications of choice. The recommended target goal of therapy is: serum uric acid level of less than 6 mg/dL, a level below the saturation point of 6.8 mg/dL at which urate crystals precipitate from solution If the patient has, or is at risk for, renal insufficiency or renal calculi (kidney stones), allopurinol is also effective at a lowered adjusted dose

Clinical Manifestations and Assessment of SLE cont'd:

Varied and frequent neuropsychiatric presentations of SLE are generally demonstrated by subtle changes in behavior patterns or cognitive ability. Mood disorder depression psychosis are common Pericarditis and pleuritis are the most common cardiopulmonary disorders. Women who have SLE are also at risk for early atherosclerosis. About 50% of patients with SLE have renal disease, such as glomerulonephritis. Serum creatinine levels and urinalysis are used in screening for renal involvement. Early detection allows for prompt treatment, so that renal damage can be prevented. Renal involvement may lead to hypertension, which also requires careful monitoring and management.

osteophyte:

a bony outgrowth or protuberance; spur

articulation:

a joint; site of close approximation of two or more bones

Treatment of RA:

can be simple, aimed at localized relief or it can be complex, directed toward relief of systemic effects Educate patient Arthritis Foundation for support Therapeutic program compatible w/ lifestyle Pharmacologic intervention (especially early in disease process) Pharmacologic management: manage symptoms control pain & inflammation and—in some diseases, such as rheumatoid arthritis (RA)—modify the disease course. Selection of medication is based on the patient's needs, the stage of disease, and the risk of side effects. Antiarthritic drugs fall into three major groups: 1) nonsteroidal anti-inflammatory drugs (NSAIDs) including salicylates (e.g., aspirin) 2) disease-modifying antirheumatic drugs (DMARDs) 3) glucocorticoids (adrenal corticosteroids) Nonpharmacologic treatment measures include: use of heat or cold weight reduction joint rest and avoidance of joint overuse orthotic devices (e.g., splints, braces) to support inflamed joints an exercise regimen Other nonpharmacologic modalities such as: massage yoga pulsed electromagnetic fields transcutaneous electrical nerve stimulation (TENS) music therapy have been used in the treatment of arthritis. In addition: iontophoresis can be used to deliver medication through the skin using direct electrical current. Common complementary and alternative medicine (CAM) choices used by rheumatologic patients include: dietary supplements herbal therapies mind/body and spiritual practices manual/manipulative therapies biostimulation topical ointments

Clinical Manifestations and Assessment of OA:

general clinical manifestations of OA are: -pain -stiffness -loss of movement and function -Pain in one or more joints typically is worsened by activities and is alleviated by rest -OA pain is unusual during the night or at rest, there are exceptions -Stiffness may occur in the morning, after a period of inactivity, or particularly in the evening -Morning stiffness usually resolves after less than 10 minutes (no more than 30 minutes duration), in contrast to prolonged stiffness seen in inflammatory disorders -Functional impairment is reflected in limited range of motion (ROM) and patient report of limited ability to perform day-to-day activities -OA is typically diagnosed by an overall clinical impression based on the patient's age and history, location of joint abnormalities, and radiographic findings -**Limited passive movement can be the first and only physical sign of symptomatic OA During joint examination: -crepitus, a continuous grating sensation, may be felt or heard as the joint goes through ROM. -joint enlargement, resulting from joint effusion or bony swelling or both. This is most easily detected in knees by the evidence of patellar tap or by the elicitation of a fluid thrill (wave test) -Joint deformities reflect advanced disease with joint destruction, which then contributes to misalignment, joint instability (causing a sensation in the knees of "giving way" or "locking"), and limb shortening. -Fingers also can be misaligned in the presence of Heberden's-close to nail (enlargements of DIP joints) or Bouchard's nodes-middle/main knuckle (enlargements of PIP joints)

podagra:

gout, especially of the great toe

Clinical Manifestations and Assessment of SLE:

onset may be insidious or acute Systemic and musculoskeletal manifestations, particularly fatigue and myalgias/arthralgias, are most prevalent (95%) in the course of the disease Clinical manifestations can resemble RA and may be mistaken for it in early course of the disease. Unlike RA, the arthritis is nonerosive and not seen on X-ray. Skin manifestations are: Photosensitivity rashes are most common Most characteristic skin manifestation is an acute cutaneous lesion consisting of a butterfly-shaped rash across the bridge of the nose and cheeks. This malar rash manifests as an erythematous, flat or raised lesion, pruritic (itchy) or painful, and can be transient and heal without scarring. In some cases of discoid lupus erythematosus (DLE), only skin involvement occurs. Discoid (coinlike) lesions are scarring and ring-shaped that may result in erythematous, scaling plaques and alopecia (hair loss). In some patients with SLE, the initial skin involvement is the precursor to more systemic involvement. The lesions often worsen during exacerbations (flares) of the systemic disease and possibly are provoked by sunlight or artificial ultraviolet B light. RN ALERT- The nurse should teach patients to avoid sunlight or ultraviolet (UV) exposure and to protect themselves with sunscreen, at least a sun protection factor of 30, and clothing.

synovial:

pertaining to a complex joint bounded by joint capsule and containing synovial fluid *synovitis: inflammation of the synovial membrane

definitive diagnosis of gouty arthritis is established by:

polarized light microscopy of synovial fluid AKA: a microscope of aspirated synovial fluid

Erythrocyte Sedimentation Rate (ESR)

reflects inflammatory activity and, indirectly, the progression or remission of disease. Ultimately, the provider determines which tests are necessary based on the symptoms, stage of disease, cost, and likely benefit of the test. The ESR measures the rate in which red blood cells (RBCs) suspended in plasma fall in a test tube. Increased "sed" rates are often associated with inflammatory states. Normally, the distance a RBC falls in 1 hour is less than 15 mm/hr for men and slightly higher in women. The speed with which the RBC moves is related to the clumping of RBCs. The more clumping, the heavier and higher the speed that a RBC falls. Inflammatory states produce proteins that encourage this clumping, thus high ESR levels are associated with inflammation. The ESR does not diagnose a problem, but it is used to monitor status of a disease and response to therapy Erythrocyte Sedimentation Rate (ESR) Measures the rate at which red blood cells settle out of unclotted blood in 1 hour Normal Value: Westergren's Method Men, 0 to 15 mm/hr, over age 50 years: 0 to 20 mm/hr Women, 0 to 20 mm/hr, over age 50 years: 0 to 30 mm/hr Implications: Increase is usually seen in inflammatory connective tissue diseases (e.g., RA, SLE, scleroderma), gout, can be seen in elderly An increase indicates rising inflammation; the higher the ESR, the greater the inflammatory activity

Pathophysiology of Scleroderma:

remissions and exacerbations Systemic scleroderma is a progressive, chronic, devastating, and debilitating disease with a prognosis not as optimistic as that of SLE. Three cardinal features: -vascular injury and damage -activation of innate and adaptive arms of the immune system autoimmunity -generalized interstitial and vascular fibrosis. Commonly begins with skin involvement. Initially, the inflammatory response causes: -edema formation, with a resulting taut, smooth, and shiny skin appearance. The skin then undergoes: -fibrotic changes, leading to loss of elasticity and movement. Eventually, tissue degenerates and becomes nonfunctional. This chain of events, from inflammation to degeneration, also occurs in: -blood vessels -synovium -skeletal muscles -internal organ(s) of the heart, lungs, GI tract, and kidneys

arthroplasty:

repair of joint problems through the operating arthroscope (an instrument that allows the surgeon to operate within a joint without a large incision) OR, through open joint surgery

Commonly called arthritis (inflammation of a joint), rheumatic diseases :

symptoms that most commonly causes a person to seek medical attention is: pain. Other common symptoms include: joint swelling, limited movement, stiffness, weakness, and fatigue onset can be acute or insidious & there are periods of remission & exacerbation Assessment includes: complete health history complete physical examination functional assessment Inspect patient's general appearance, gait, posture, general musculoskeletal size, and structure are observed. Gross deformities and abnormalities in movement are noted. The symmetry, size, and contour of other connective tissues, such as the skin and adipose tissue, are recorded. Observation of activities is made: the patient demonstrates what he or she can and cannot do, such as dressing and getting in and out of a chair. Observation includes: adaptations and adjustments the patient may have made (sometimes without awareness); for example, with shoulder or elbow involvement, the person may bend over to reach a fork, rather than raising the fork to the mouth.

Despite the diversity of rheumatic disorders:

the joint is the area most commonly affected and involves some degree of inflammation and damage to the articular cartilages, which may occur simultaneously