1247 Musculoskeletal

Biphosphonates: alendronate/Fosamax, & ibandronate/Boniva

(Osteoporosis) Inhibit osteoclast-mediated bone resorption thereby increasing BMD and total bone mass. SE: anorexia, weight loss, gastritis, esophageal irritation Patient Teaching: Take on an empty stomach, in a.m., at least 30 minutes before any food, beverages or medications. Do not take within 2 hours of any calcium- containing food. To decrease esophageal irritation - take with a full glass of water, remain upright for at least 30 minutes after taking the medication.

teriparatide/Forteo: recombinant form of human PTH

(Osteoporosis) increases action of osteoblasts in treatment of osteoporosis; first drug approved that STIMULATES new bone formation rather than inhibiting bone loss; SubQ once/day. SE: leg cramps, dizziness; TEACH to report bone pain or leg cramps, which can be d/t imbalanced serum CA levels

Explain how each of the following classification of medications assist in treating SLE. NSAIDS: Corticosteroids: Steroid-sparing drugs - (Methotrexate): Antimalarials - (Plaquenil): Immunosuppressive:

*NSAIDS: very important in those with mild polyarthralgias or polyarthritis, carefully monitor for adverse GI effects *Corticosteroids: useful in controlling severe exacerbations of polyarthritis, exposure should be limited; SINGLE MOST IMPORTANT med to use *Steroid-sparing drugs - (Methotrexate): alternative treatment prescribed in combination with folic acid to decrease minor side effects of corticosteroids *Antimalarials - (hydroxychlogoquine/Plaquenil): to treat fatigue and moderate skin and joint problems, response may not be noticed for several months *Immunosuppressive: (cyclophosphamide/Cytoxan, mycophenolate mofetil/CellCept) prescribed to reduce the need for long-term corticosteroid therapy

Why is osteoporosis more common in women than in men (5 reasons)? What are additional risk factors?

1) Women tend to have lower calcium intake than men throughout their lives 2) women have less bone mass because they generally have a smaller frame 3) bone resorption begins at an earlier age in women and is accelerated at menopause (loss of estrogen) 4) pregnancy/breastfeeding deplete a woman's skeletal reserve unless calcium intake is adequate 5) longevity increases likelihood of osteroporosis >65 yrs, low body weight, white or Asian (African-A and Mexican-A have higher bone density so not as high a risk), SMOKING, inactive lifestyle, family history, diet low in calcium or Vit D, excessive use of alcohol (>2 drinks/day), long term use of corticosteroids, thyroid replacements, heparin, long-acting sedatives, or antiepileptics

RA: pathophysiology

1) antigen (not same for all patients) triggers ABNORMAL immunoglobulin G (IgG); rheumatoid factor (RF) autoantibodies respond to the abormal IgG and combines with IgG to form complexes that deposit on synovial membranes and cartilage in joints, thus stimulating activation of complement and inflammatory response. 2) Neutrophils (elevated WBC count) migrate to site (chemotaxis) and release proteolytic enzymes that damage cartilage and cause synovial lining to thicken; CD4 T helper cells stimulate monocytes, macrophages to secrete inflammatory cytokines including interleukin-1 and -6 and tumor necrosis factor (TNF). 3) Vascular granulation tissues grows across the cartilage (pannus) with loss of cartilage beneath expanding pannus; pannus causes cartilage destruction and bone erosion; joint deformities develop and bone density decreases (osteoporosis)

RA: Goals of CAre

1) control disease activity 2) relieve pain 3) maintain functionality and ADLs 4) maximize quality of life

Osteomyelitis: local manifestations

ACUTE = constant bone pain unrelieved by rest and worsens with activity; swelling, tenderness and warmth at the infection site; movement of affected part might be restricted CHRONIC = constant bone pain, swelling, warmth; over time granulation tissue turns to scar tissue, providing ideal avascular site for microbes, which ABX cannot penetrate

Osteomyelitis: systemic manifestations

ACUTE = fever, night sweats, chills, restlessness, nausea and malaise; later signs include drainage from cutaneous sinus tracts or fracture site CHRONIC = systemic are same, but may be diminished

Osteomyelitis: classifications

ACUTE: < 1 month CHRONIC: infection for > 1 month or infection that fails to respond to initial ABX tx

Osteomylitis: maintaining mobility

AFTER initial tx and when pain subsides; ROM, assist to stand and ambulate, provide assistive devices to help

Osteomyelitis: nursing care/teaching r/t meds

AMINOGLYCOSIDES (-mycins): report if tinnitus, visual disturbances or urinary problems develop; monitor fluids for retention, renal function, peaks/troughs and assess for toxicities CEPHALOSPORINS (cephalexin/Keflex, cefazolin/Ancef): watch for hives, severe/watery diarrhea, melena (blood in stool) and throat/mouth sores FLOUROQUINOLONES (ciprofloxacin/Cipro, levofloxacin/Levaquin): tendon rupture, esp. Achilles Cephalosporings & Quinolones: jaundice, colitis, photosensitivity, crystalluria (protect from sun exposure and drink lots of fluids) Monitor peak/trough for all drugs to prevent toxicity; d/t ABX length, teach to monitor for opportunistic infection (candidiasis) and C. difficile so report any white/yellow, curd lesions or GU changes such as perianal itching or diarrhea TEACH venous access device care; stress ABX adherence and f/u labs

Osteomyelitis: IV therapy meds

AMINOGLYCOSIDES (gentamicin/Garamycin, tobramycin/Nebcin, neomycin): MUST monitor nephrotoxicity, ototoxicity, optic neuritis, fluid retention issues; must do renal function (BUN/creatinine) prior and during tx; must assess vestibular and auditory function prior and 3-4 after d/c therapy; monitor peak/trough for therapeutic levels to prevent toxicity; patient must report visual, hearing or urinary problems CEPHALOSPORINS (cephalexin/Keflex, cefazolin/Ancef, cefoxitin/Mefoxin): jaundice, colitis, photosensitivity, crystalluria; C&S prior to tx PENICILLINS (penicillin, nafcilin) VANCOMYCIN: usually last resort for serious gram + infections

How do each of the following classification of medications assist in treatment of RA? ASA: NSAIDS: Corticosteroids:

ASA: Antinflammatory, analgesic, antipyretic, inhibit synthesis of prostaglandins NSAIDS: important intervention for polyarthralgia or polyarthritis; anti-inflammatory, antipyretic, inhibit synthesis of prostaglandins; COX-2 inhibitor (celecoxib/Celebrex) Corticosteroids: injections(methylprednisolone acetate/Depo-Medrol) reduce flareups, inflammation and associated pain; long-term orals (e.g., methyprednisolone/Solu-Merol) should NOT be mainstay b/c of osteoporosis and avascular necrosis

When is a wound vac used for osteomyelitis?

After debridement, the wound may be closed and negative air pressure (wound vac) may be used to draw it together; promotes angiogenesis at site d/t to continuous irritation from wound vac

Gold Compounds : gold sodium thiomalate/Myochrysine, aurothioglucose/Solganal (both parenteral) or auranofin/Ridaura (oral)

Alters immune response, suppresses synovitis Side effects: (common) Stomatitis, dermatitis, photosensitivity, proteinuria (Serious) Leukopenia, thrombocytopenia, anemia Nursing Care: Observe for pruritis, rash, sore mouth, metallic taste. Monitor CBC, UA. Therapeutic response may not occur for 3-6 months

Rheumatoid Arthritis: chloroquine/Plaquenil

Antimalarial DMARD; (Second choice of drug treatment with RA) - May suppress formation of antigens; therapeutic effect may take up to 6 months Side effects: Ocular toxicity - changes in vision, Ototoxicity - changes in hearing or tinnitus, Peripheral neuritis causing muscular weakness Nursing Care: Monitor CBC and hepatic function, Tell patient to report any above changes immediately

What are rheumatoid nodules and what problems do they cause?

Appear subcutaneously as firm, nontender, granuloma type masses located over the extensor surfaces of joints such as fingers and elbows. Nodules at the base of the spine and back of the head are common in older adults. They develop insidiously and can persist or regress spontaneously, usually not removed because of the high probability of recurrence. Can appear on the sclera or lungs which are indicative of active disease and have a poorer prognosis

Why should aspirin NOT be given to client receiving probenecid for treatment of gout?

Aspirin inactivates the effects of uricosurics, resulting in urate retention

What are supportive care measures used to protect the inflamed joints in those with gout?

Avoid careless handling. Bed rest may be appropriate with affected joints properly immobilized. Involvement of lower extremity may require use of a cradle or foot board to protect the painful area from the weight of bedclothes; local application of heat or cold

Osteomyelitis: diagnostics

BONE/TISSUE BIOPSY: definitively determines causative organism blood/wound culture: frequently positive for organisms elevated WBC & ESR: may indicate infection X-ray: signs appear 10 days to weeks after initial clinical symptoms and disease will probably have progressed radionuclide bone scans: helpful in diagnosis, usually positive MRI/CT: used to help identify extent of infection

What causes ischemia of the bone?

Bacteria invade bone causing inflammation, which creates pressure within bone d/t bone's non-expanding characteristic; pressure leads to ischemia and vascular compromise of periosteum leading to bone necrosis

Biologic/Targeted therapy (TNF ihibitors) for RA: etanercept/Enbrel, infliximab/Remicade, adalimumab/Humira

Bind to TNF, thus blocking interaction with TNF cell receptors; Used to decrease inflammatory process and slow disease process (RA). Increased risk of TB (advise yearly PPD tests); Monitor for infection, bleeding, malignancies. Report persistent fever, it may be the only sign of an infection. Assess for signs of CHF. NO live virus vaccines during treatment

Why is osteoporosis called the "silent disease"? Is it possible to prevent osteoporosis?

Bone loss occurs without symptoms. Can prevent, but requires adequate calcium intake, e.g., 1000mg/day premenopausal or 1500 mg/day for postmenopausal women who are NOT receiving supplemental estrogen, adequate vitamin D for absorption, moderate amounts of exercise (aerobic; NOT impact aerobics) and weight-bearing exercises that build up and maintain bone mass DECREASE risks esp., by smoking cessation and decreased ETOH

What diagnostic tests are used to confirm the diagnosis of osteoporosis?

Bone mineral densitometry (BMD), which includes Dual-energy X-ray Absorptiometry (DEXA) and Quantitative Ultrasound (QUS); both assess mass and bone loss DEXA reports T-scores (number of standard deviations below avg. normal bone density); -1 or higher = normal; -1 to -2.5 = osteopenia and -2.5 and lower = osteoporosis

What are the clinical manifestations related to multisystem involvement in SLE? Why do they occur?

CHRONIC multisystem autoimmune disease involving vascular and connective tissue; typically affects: SKIN (discoids of round, coin-shaped skin lesions; "butterfly rash" of face, photosensitivity, alopecia, mouth/esophageal ulcers, dry/scaly scalp) Musculoskeletal: joints (arthritis, polyarthralgia), synovitis, myositis (muscle pain), fatigue CARDIO/PULMONARY: pleuritis, pericarditis, pleural effusion, Raynaud's, tachypnea GU: proteinuria, lupus nephritis (LN), glomerulonephritis NEUROLOGIC: focal seizures, peripheral neuropathy, organic brain syndrome, psychoses GI: diarrhea, N/V, dysphagia Hematologic: anemia, leukopenia, thrombocytopenia, lymphadenopathy Generalized: fatigue, low-grade fever, loss of appetite, weight loss, increased susceptibility to infection SLE mostly affects women in childbearing years; women 10X more likely to develop than men; NO characteristic pattern occurs in the progressive involvement, any organ can be affected by an accumulation of circulating immune complexes.

How do the following mediations assist in the treatment of gout? Colchicine: Xanthine-oxidase inhibitors : Ucosurics:

COLCHICINE: treatment for acute gouty arthritis. Provides antiinflammtory effect but no analgesic, NSAID is added with treatment for pain management. Generally produces dramatic pain relief within 12-24 hours of attack; this med ONLY works on gout, so therapeutic results provide further evidence for gout diagnosis XANTHINE-oxidase inhibitors : decrease uric acid production; used for gout maintenance; force fluids (2-3 L) on these meds to prevent precipitation in renal tubules and to keep urine alkaline allopurinol/Zyloprim: esp. good for pt with uric acid stones or renal impariment; but can lead to agranulocytosis febuxostat/Uloric: long-term mgmt of hyperuricemia in those with chronic gout UCOSURICs: inhibit renal tubular reabsorption of urates; increase uric acid excretion in urine; probenecid (Benemid) and sulfinapyrazone (Anturane) : INEFFECTIVE when creatinine clearance is reduced (occurs in 60 y.o. or more; those with renal impairment); do NOT take ASA, as it inactivates effects; acetaminophen may be taken

What it the purpose of hyberbaric oxygen in treatment of osteomyelitis?

Can be given as an adjunct therapy in refractory cases of chronic osteomyelitis. Thought to stimulate circulation and healing of the tissue

Why do patients with chronic gout often develop kidney disease?

Contributes to polynephritis associated with intrarenal sodium urate deposits and obstruction

SLE: Goals of Therapy

Control inflammation, Provide emotional support, and develop a life plan

What is the single most important medication used in the treatment of SLE?

Corticosteroids

Osteomyelitis: Direct Entry

Doccurs at any age through open wound when organisms can gain entry into body. May also occur in presence of foreign body (implants, prosthetic device). Microorganisms gain entrance to bone via blood through wound, lodge in area of slower circulation (metaphysis), and grow causing increase in pressure which leads to ischemia and bone death.

Osteomyelitis: goals of care

Halt the infection, Relieve pain and Maintain Mobility (after initial tx and pain decreases--ensure mobility with ROM, assisting to stand and ambulate with assistive devices)

What foods are high in calcium? What foods are poor calcium sources? Why is vitamin D important in treatment of osteoporosis?

High = yogurt, almonds, skim milk, whole milk, spinach (cooked is more concentrated), ice cream, American cheese, salmon, chedder/cottage cheese, broccoli, sardines, oysters (ALL are PER serving and in order from highest to lowest calcium content) Poor calcium sources = egg, beef, pork, poultry, apples, bananas, potato, lettuce, carrot Vit D is important in calcium absorption and function, may also have a role in bone formation

What is pannus and how does it develop in rheumatoid arthritis?

Highly vascular granulation tissue Joint changes from chronic inflammation begin when the hypertrophied synovial membrane invades the surrounding cartilage, ligaments, tendons and joint capsule. Pannus forms within the joint and eventually covers the entire surface of the articular cartilage; pannus causes focal destruction of bone

SLE: What are important concepts to include in patient and family teaching and related nursing care?

Increase Mobility: ROM, assistive devices - walkers, canes, crutches, braces, splints and firm mattress Facilitate self-care: Provide adaptive equipment for eating, bathing (avoid drying soaps, powders, household chemicals), toileting, dressing; apply heat/cold therapy; avoid others with infection Conserve energy by pacing activities. Allow patient extra time to complete care. Improve body image: Encourage patient to verbalize feelings, perceptions, and fears Monitor for complications: Assess for serious adverse effects of medications used in treatment. Avoid immunizations with live viruses

What are the three major signs and symptoms of osteoarthritis?

Joint Pain (arthralgia), Joint Stiffness, Crepitation (grating sensation caused by loose cartilage particles)

What are complications of RA?

Joint destruction - flexion contractures and hand deformities, nodular myositis and muscle fiber degeneration, cataracts, pressure ulcers, pleurisy, pleural effusion, pericardial effusion, cardiomyopathy, carpal tunnel syndrome

RA and OA: principle differences

LOCAL: OA (joint pain is predominate symptom; early morning stiffness usually resolves in 30 min; joints affected asymmetrically) vs RA (morning stiffness does not resolve easily; joints affected symmetrically SYSTEMIC: OA (NONE) vs RA (fatigue, fever, organ involvement)

What nursing care and patient teaching is important for medications used in osteomyelitis treatment?

Measure peak and trough levels, dosages are adjusted to maintain peak levels (and to prevent oto- or nephro-toxicity with aminoglycosides) Preventive measures: Monitor I & O (kidney function problems). Keep patient well hydrated to prevent nephrotoxicity or crystalluria. Avoid direct sunlight, wear sunscreen. Monitor urinary function, hearing, vision. Assess for signs of yeast infections in genitourinary tract and mouth.

Explain why Methotrexate (Rheumatrex) is know as the cornerstone medication in treating RA. What are the side effects? What are important nursing implications?

Methotrexate (Rheumatrex): is a Disease modifying antirheumatic drug or DMARD; antimetabolite - inhibits DNA, RNA, protein synthesis; rapid antiinflammatory effect, which reduces symptoms in days to weeks; lower toxicity than other drugs. Side effects: hepatotoxicity and bone marrow suppression; Small dose and different administration schedule make it less likely that patient will develop symptoms related to drugs antineoplastic activity (GI and skin toxicity, bone marrow depression, nephropathy) Considerations: Monitor CBC and hepatic and renal function. Advise patient to report signs of anemia (fatigue, weakness). Keep patient well hydrated. Teratogenic effects. Inform female patient that contraception should be used during and 3 mo. after treatment

Selective Estrogen Receptor Modulator: raloxifene/Evista

Mimics effect of estrogen on bone by reducing bone resorption and does NOT stimulate breasts or uterus (important to remember as it r/t breast and uterine cancer); may actually DECREASE breast cancer risk. Increases osteoblasts and bone mineral density. SE: Leg cramps, hot flashes, blood clots

RA: Joint protection

Modify tasks to lessen stress on joints; work in short periods with scheduled rest breaks to avoid fatigue. Sit when doing tasks whenever possible; push up with palms instead of fingers; Spread chores throughout the week rather than all at one time. Delegate chores. Perform ROM; use lightweight splints to prevent contractures; avoid going up and down stairs repeatedly. Avoid repetitious/long-term movements; use time saving joint protective devices (ex: electric can opener, velcro fasteners, zippers, buttonhooks)

How is the effectiveness of drug therapy monitored for osteomyelitis?

Monitored through bone scans and ESR tests, as well as relief from symptoms

What are the major patient teachings to assist the patient living with osteoarthritis?

NO cure. 1) MANAGE pain (and inflammation d/t secondary causes, e.g., synovitis); inflammation is usually NOT characteristic of OA 2) PREVENT disability 3) MAINTAIN joint function. Non-drug interventions are FOUNDATION of treatment: Rest during acute inflammation (not to exceed 1 week immobilization); Heat (long-term) and Cold (acute inflammation) for pain/stiffness; Weight reduction (if overweight) and supplements (glucosamine and chondroitin) ROM, aerobic conditioning; Complementary and Alternative Therapies - acupuncture, yoga, massage, guided imagery, therapeutic touch; Ease tasks; use assistive devices; good posture/proper body mechanics MEDICATIONS: Acetaminophen; NSAIDS; COX-2 inhibitors (reduce GI problems) intraarticular corticosteroids (Depo-Medrol), Immunosuppresants that inhibit DNA/RNA synthesis (azathioprine/Imuran); Biologic/Targeted therapy which bind to TNF and block TNF cell receptors, thus reducing inflammatory/immune response (infliximad/Remicade, adalimumab/Humira); Topicals (capsaicin cream/Zostrix or Capzasin-P) which block pain; Hyaluronic acid (HA), which contributes to viscosity and elasticity of synovial fluid SURGERY: arthroscopic to remove debris or arthroplasty to rebuild

Describe the anticipated findings for each of the following diagnostic tests for a patient with SLE. *Antinuclear antibody (ANA), Anti-Smith antibody (Anti-Sm), Anti-DNA antibody *ESR & CRP *LE cell prep

NO specific test for diagnosing SLE. *Antibody testing: Antinuclear antibody (ANA present in 97% of cases), Anti-Smith antibody (Anti-Sm in 30-40%; seems to be found almost exclusively in SLE), Anti-DNA antibody (establishes the existence of an autoimmune disease). *ESR & CRP: elevated, may be used to monitor disease activity and effectiveness of therapy, though anti-DNA titers are more important for disease monitoring *lupus erythematosus (LE) cell prep: NON-specific test for SLE; can be positive in other rheumatic diseases

Osteoarthritis (OA): clinical manifestations

NO systemic manifestations, which is important distinction between OA and other inflammatory joint disorders such as RA JOINTS: mild discomfort to significant disability; pain worsens with use and relieved by rest in EARLY stages; (in ADVANCED stage pain rest and use both have pain); sleep disruptions d/t pain, pain worsens when barometric pressure falls, pain may refer, getting up & down difficult; most commonly-affected joints are distal interphalangeal (DIP; typically called Heberden's nodes) and proximal interphalangeal (PIP, typically called Bouchard's nodes) of fingers, metacarpophalangeal (MCP) of thumb, weight-bearing (hips/knees) and cervical/lumbar vertebrae

bone cells & functions

OSTEOBLASTS: secrete and lay down bone matrix, which provides framework for mineral deposits of calcium and phosphorus OSTEOCYTES: mature bone cells in matrix; bone maintenance OSTEOCLASTS: dissolve (break down) and resorb bone

Why are bone infections difficult to eradicate?

Once new bone forms (involucrum), a sequestrum continues to be an infected island of bone surrounded by pus (abscess). It makes it difficult for blood-borne antibiotics or WBCs to reach the sequestrum

What is the difference between primary and secondary gout? What is hyperuricemia?

Primary = inherited error in purine metabolism leads to overproduction or retention of uric acid, 90% of cases Secondary = result of drugs known to inhibit uric acid excretion Hyperuricemia: high uric acid levels in the blood

Immunosuppressants for RA: azathioprine/Imuran, cyclophosphamide/Cytoxan

RA meds that inhibit DNA, RNA, protein synthesis Assess for GI irritation. Advise patient to report unusual bleeding or bruising. Increase fluid intake. Avoid during pregnancy. Therapeutic response may take up to 12 wks

How does the autoimmune theory explain the etiology of rheumatoid arthritis?

RA probably triggered from combination of genetics and environment; thought to begin when susceptible person has initial immune response to antigen, e.g., bacterium or virus; strongest genetic evidence is role of human leukocyte antigens (HLA), esp. HLA-B27 (HLAs are also associated with DM type 1); smoking increases risk for predisposed patients

RA: How do these assist with preventing pain and deformities? Rest and Good body alignment: Heat and cold therapy: Exercise: Nutrition:

Rest/Good body alignment: Alternate rest periods with activity, sleep at least 8-10 hours/night. Firm mattress or bed board (alignment). Splints and casts (promote rest/support and maintain alignment) can be helpful and positions of extension should be encouraged. Lying prone for 30 min/ twice daily is recommended. NEVER place pillows under the knees (joint contracture). Heat/Cold: plan around morning stiffness; relieve stiffness, pain and muscle spasm, ice especially during periods of exacerbation- no more than 15 min at one time; warm showers, warm towels, soaking hands in warm water may relieve stiffness and improve ability to perform ADLs; never apply heat > 20 min Exercise: ROM done daily to keep joints functional, therapeutic exercise usually developed by PT improves flexibility and strength of the affected joints and patients overall endurance Nutrition: no special diet, but balanced nutrition important d/t anorexia from fatigue, pain, depression

What are the extraarticular manifestations of RA?

Rheumatoid nodules (20-30% of patients) are firm, nontender, granuloma-type masses that may ulcerate; Sjogren's syndrome is diminished lacrimal and salivary gland secretion (dry mouth, burning/itching eyes) and Felty syndrome(splenomegaly and leukopenia)

How is a definitive diagnosis of gout determined?

Serum Uric acid - elevated ; usually above 6 mg/dl -not specifically diagnostic WBC- elevated as high as 20,000/mm3 during acute attack ESR: elevated Synovial fluid aspiration: only possible to diagnose in 80% of patients, BUT only reliable test to distinguish gout from septic arthritis and pseudo-gout (calcium phosphate crystal formation) 24 hour urine collection-determine uric acid production and excretion (evaluate if from decreased renal excretion or overproduction of uric acid) ****Most commonly diagnosed via clinical symptoms such as Tophi, which indicates chronic disease

Name foods with purine that the patient should avoid.

Shellfish (crab, shrimp), lentils, asparagus, spinach, beef, chicken and pork; also eat low-fat, low-calorie foods and avoid ETOH (may precipitate)

SLE & impaired skin integrity: What should be taught to minimize this effect of the disease?

Skin issues = alopecia, photosensitivity, rash, lesions. Apply topical anti-inflammatory. Avoid direct sunlight. Use sunscreens and protective clothing, sun hats with minimal sun exposure 11a-3p

In acute interventions, how is the affected limb protected in osteomyelitis?

Some immobilization (splint, traction) to decrease the pain. Carefully handle the involved limb and avoid excess manipulation, which increases pain and may cause pathologic fracture. Give meds: NSAID'S, opioid analgesics, muscle relaxants

What are the clinical manifestations of gout?

Stage 1: asymptomatic; hyperuricemic Stage 2: acute gouty arthritis - affect single joint, usually great toe PAIN, excruitating, starts at night; Hot, swollen; will have fever for 2-10 days; big toe usually first joint affected Stage 3: Development of Tophi - deposits of sodium urate crystals develop in multiple areas (esp. ear, elbows, hands, toes) compress nerves and erode through tissues

DMARD for RA treatment: suflasalazine/Azulfidine

Sulfonamide- anti-inflammatory (blocks PG synthesis) Side effects: GI effects (anorexia, nausea, vomiting), bleeding, bruising, jaundice, HA, rash, pruritis Considerations: Drug may cause orange-yellow discoloration of urine or skin. Space doses evenly around the clock, take drug after food with 8 oz. of water. Monitor CBC; treatment may continue even after symptoms improve

Chronic osteomyelitis: treatment

Surgical removal of poorly vascularized tissue/dead bone followed with extended ABX use. IV therapy, but oral Fluoroquinolones (-oxacins) for 6-8 weeks may be prescribed instead; may irrigate wound with ABX and use wound vac to draw wound together (assess wound and drainage); hyperbaric oxygen may also be given (stimulates circulation, heals tissue); bone grafts; amputation, if indicated

What are the clinical manifestations of Rheumatoid Arthritis (RA)? How does Rheumatoid arthritis affect joints?

Systemic: Fatigue, Anorexia, Weight loss, Generalized stiffness, Local: Joints are tender, painful, stiff, swollen and warm to touch; joint symptoms are symmetrical; frequently attacks wrists, hands (small joints usually attacked first), elbows, shoulders, knees and ankles; morning stiffness that can last an hour or more; joint pain increases with movement; tenosynovitis (inflammation of fluid-filled sheath surrounding tendon); Rheumatic nodules Destroys joints; causes joint deformities (as RA progresses, inflammation & fibrosis of joint capsule and supporting structures lead to deformity/disability); causes cartilage and bone density loss; subluxation; typical deformities include hallux valgus (toe bunion), swan neck in fingers, ulnar drift, boutonniere deformity (hand) LATE SYMPTOMS: Pallor, Anemia, Color changes of digits (bluish/ pallor), Muscle weakness, atrophy; paresthesias, contractures, subluxation, dislocation

Explain the "causes" (etiology) of systematic lupus erythematosus (SLE)?

The precise reason for the abnormal autoimmunity that causes lupus is unknown: Inherited genes (multiple susceptibility genes from the human leukocyte antigen complex, including HLA-DR3), viruses, UV light, Dozens of medications have been reported to trigger SLE; hormones play a role as onset/exacerbations occur at menarche, with OC use and during/after pregnancy

When is debridement used? What are ways that antibiotics are directly placed in the wound?

To prevent further infection and promote healing in chronic osteomyelitis Antibiotic-impregnanted polymethylmethacrylate bead chains are implanted to aid in combating infection; wound can also be irrigated with antibiotics

Why is a high fluid intake very important for the patient with gout?

To prevent precipitation of uric acid in the renal tubules - (2-3 L/ day)

Acute osteomyelitis: treatment of choice

Vigorous, prolonged IV ABX therapy is treatment of choice. (Do C&S firs,t as with all ABX therapies.) Oral fluoroquinolones (-oxacins) MAY also be prescribed orally for 6-8 weeks AFTER IV tx to ensure resolution; if ABX tx delayed, surgical debridement and decompression often necessary; IV therapy usually 4-6 weeks, but as long as 3-6 months; usually via CVAD (PICC or percutatneous non-tunneled); patients need to care for CVAD; skilled nursing facility f/u for 6 months after discharge. Fluoroquinolones may be used for ORAL tx for 6-8 weeks (instead of IV) or after IV tx of acute infection; beware of tendon rupture risk with fluouroquinolones

Osteoarthritis: diagnostics

X-rays confirm and stage OA. Bone scan, CT or MRI useful b/c of sensitivity in detecting early joint changes; transient elevation in ESR r/t synovitis

Osteoporosis: definition

aka porous bone disease; chronic, progressive metabolic bone disease characterized by low bone mass and structural deterioration of bone tissue; normal remodeling altered as bone resorption > bone formation

Gout: Complications

assess for kidney stones, hypertriglyceridemia, HTN

RA: disease-modifying antirheumatic drugs (DMARD)

b/c irreversible joint changes can occur as early as first year of RA, DMARDs are aggressively prescribed; potential to less permanent effects, i.e., joint erosion and deformity

Osteomyelitis: acute intervention care during bedrest

bed rest frequent, so good body alignment and frequent position changes; PREVENT contractures (pt. typically flexes to promote comfort) at hips and foot (foot drop)

Chronic Osteomyelitis

bone infection that persists for longer than 1 month or that has not responded to antibiotic therapy. Systemic signs may be diminished, local signs of infection more common (bone pain, swelling, tenderness, warmth at site); over time granulation tissue at site turns into avascular scar tissue, providing idleal site for microorganisms that cannot be penetrated by ABX

What happens to the joints in osteoarthritis?

cartilage erodes in the synovial joints, leading to the formation of new joint tissue; cartilage repair does not keep up with rate of destruction allowing fissures and erosion; bony growths (osteophytes) develop in uneven distribution, which cause stress, friction and reduction in motion; typically affects joints of fingers and thumb, hip, knee, foot joint and cervical or lower lumbar vertebrae

Bone composition

cells, protein and mineral deposits

SLE: pathophysiology

characterized by production of large variety of autoantibodies against nucleic acids, e.g., single- or double-stranded DNA (known as anti-DNA antibody), erythrocytes, coagulation proteins, lymphocytes, platelets; autoimmune reactions characteristically are directed against cell nucleus (know as anti-nuclear antibodies or ANAs); circulating immune complexes containing ANA deposit in basal membranes of capillaries in kidneys, heart, skin, brain and joints where complement is activated and inflammation occurs; overaggressive autoimmune response is also r/t activation of B and T cells

Rheumatoid Arthritis (RA)

chronic, systemic autoimmune disease characterized by inflammation of connective tissue in the diarthrodial (synovial) joints, typically with periods of remission and exacerbation; frequently accompanied by extraarticular (systemic) manifestations. Women more likely to have RA; affects all ethnic groups; risk increases with age, peaking between 30 and 50 years old; increased stress linked; family history might be genetic link

bone remodeling

constant state of turnover between formation and resorption; aim is to provide maximum strength with minimal mass AND to provide source of mineral ion homeostasis; balance is influenced by physical activity (weight bearing), dietary calcium/vitamin D, PTH, estrogen and bone supply

Osteoporosis: Nursing Care

encourage diet high in calcium (food and/or supplements), encourage regular weight-bearing exercises (walking, hiking, weight-training, stairs, dancing, tennis, but NOT high-impact, e.g., running, which may stress bones), decrease risk factors, e.g., smoking, ETOH

Osteoporosis: calcium supplements

if diet inadequate, use supplements from various sources, including Tums; should take with vitamin D to aid in absorption; difficult to absorb more than 500 mg/dose, so divide for dosing throughout day if taking large doses

Osteomyelitis: pain relief

immobilize affected limb and handle carefully to decrease pain; meds may include NSAIDs, opioids and muscle relaxants

Acute Osteomyelitis

initial infection or an infection of less than 1 month in duration; manifestations are systemic and local—fever, night sweats, chills, restlessness, nausea, malaise, constant bone pain unrelieved w/ rest, swelling/tenderness/warmth at site, restricted movement of affected part.

Osteomyelitis: direct and indirect entry

microorganisms invade directly or indirectly DIRECT: occurs at any age in presence of open wound (e.g., fractures, penetrating wounds, pressure ulcers) when microbes may penetrate; may also occur in presence of foreign body (implant, plate, prosthesis) INDIRECT (hematogenous--spread via blood): occurs most frequently in growing bones of boys younger than 12 and associated with blunt trauma; adults with vascular insufficiency (DM, PAD, atherosclerosis) and GU or respiratory infections at higher risk

Osteoporosis: clinical manifestations

most common in spine, hips, wrists; initial manifestations are back pain, spontaneous fractures or minimal trauma fractures

Involucrum

new bone that forms in the periosteum that continues to have blood supply; usually forms around a sequestrum

Osteoporosis: estrogen therapy after menopause

no longer given as primary tx d/t risk of heart disease and breast/uterine cancer, but sometimes prescribed for short duration for specific benefits; estrogen believed to inhibit osteoclasts

Osteomyelitis: Indirect Entry

osteomyelitis invasion classification; most frequently affects growing bone in boys < 12 y.o. & associated w/ higher incidence of blunt trauma.; blunt trauma in older adults; Common sites distal femur, proximal tibia, humerus, radius. Adults w/ vascular insufficiency disorders/GU/upper respiratory infections at higher risk. Adult sites pelvis, tibia, vertebrae r/t high vascularity.

denosumab/Prolia

osteoporosis medication; postmenopausal women at high risk for fractures; monoclonal antibody that binds to a protein (RANKL) involved in formation/function of osteoclasts; subQ q 6 months

Gout: Alternative Meds for Tx other than colchicine, allopurinol or febuxostat

pegloticase/Krystexxa: patients not responding to xanthine oxidase inhibitors; drug is an enzyme that metabolizes uric acid; IV use only corticosteroids: acute gout or when other tx ineffective or contraindicated losartan/Cozaar: angiotensin II receptor antagonist promotes urate diuresis and lowers HTN (a risk for gout)

Osteoporosis: management of corticosteroid patients

prescribe lowest dose of steroids; ensure adequate calcium and vitamin D intake; if osteopenia on bone densitometry, then bisphosphonates may be added

ossification

process by which bone matrix (collagen fibers) is formed and hard mineral crystals of calcium and phosphorus are bound to the collagen

minerals in bone

provide strength and rigidity to matrix onto which they are deposited; CALCIUM: absorbed in GI tract d/t function of vitamin D PHOSPHORUS:

Osteomyelitis

severe infection of the bone, bone marrow and surrounding soft tissue; most common infecting organism is staph aureus. Organisms can invade by indirect/direct entry.

Sequestrum

the area of devitalized (dead d/t ischemia) bone that eventually separates from surrounding living bone; infections trapped inside sequestra cause recurring abscesses

calcitonin (salmon calcitonin/Calcimar)

thyroid hormone; inhibits osteoclastic bone resorption by interacting with osteoclasts. Slows rate of bone destruction, increasing calcium storage in bone and decreases the amount of calcium released into the blood; increases renal secretion of calcium & phosphorus; injected IM, subQ or intranasally

Gout: Definition and Causes

type of recurring acute arthritis characterized by accumulation of uric acid crystals in one or more joints; incidence in African-Amer. men is 2X white men; primary gout is 90% of cases and occurs predominately in middle-aged men Etiology: uric acid is major end product of purine catabolism and primarily excreted by kidneys; increase in uric acid production, underexcretion (major cause) or increased purine foods (metabolized into uric acid) are causes; high food intake alone is rarely a cause, but a precipitater of acute attack in those susceptible to gout Risks: obesity, HTN, diuretics, excessive ETOH, excessive purines

Arthritis: definition

type of rheumatic (rheumatism is non-specific term for disorders affecting joints and connective tissue) disease, which involves inflammation of a joint or joints; most common types are osteoarthritis, rheumatoid arthritis and gout

Osteoarthritis: causes

usually caused by a known event or condition that damages cartilage or causes joint instability: trauma, repetitive physical activities (common cause), inflammation (and subsequent enzyme release), neurologic disorders, skeletal deformities, drugs (indomethacin, colchicine and corticosteroids stimulate collagen-digesting enzymes); majority of adults affected by age 40; more women than men affected after 50

Tophi

visible, painless nodules filled with uric acid crystals; usually appear around joints

What specific diagnostic tests are used to confirm the diagnosis of RA?

↑ Rheumatoid factor (RF) - 80% of patients are positive and titers rise during active disease (but only occurs in 80%, so not definitive) ↑ Erythrocyte sedimentation rate (ESR) ↑ C-reactive protein (CRP) indicates active inflammation ↑ WBC (>20,000/uL) from SYNOVIAL fluid and NOT CBC ↑ anti-citrullinated protein antibody (ACPA): more specific than RF test; may allow for earlier/more accurate diagnosis Synovial fluid analysis shows straw-colored fluid with fibrin flecks and/or elevated MMP-3 enzyme and/or elevated WBC (esp. neutro) X-rays: Will not diagnosis - only show bone changes bone scan (radioisotope study - isotope given 2 hrs prior to procedure; empty bladder; must lie supine for 1 hour; no pain/harm from isotopes; increase fluids post-procedure) useful in detecting early joint changes and confirmation Diagnosis is based on the joint involvement (number and type, i.e., large/small) and positives in RF