NSG210 Hinkle Ch. 34: Assessment and Management of Patients With Inflammatory Rheumatic Disorders

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 34, pp. 1067-1092 (textbooks/HINKLE_MS_CH34.pdf, also in textbooks/exam03/). Week 08 reading (Oct 14 lecture, alterations in activity and rest); on Exam 3. Numbering note: the raw lecture plan lists “Ch. 35 - Rheumatoid Arthritis, SLE, Gout,” but in the 15th edition Ch. 35 is musculoskeletal assessment; RA, SLE, and gout are in Ch. 34. Osteoarthritis is not in this chapter; it is in Ch. 36 (nsg210-hinkle-ch36-musculoskeletal-disorders).

Learning Outcomes

1. Explain the pathophysiology of inflammatory rheumatic diseases and describe the assessment and diagnostic findings.
2. Use the nursing process as a framework for care of the patient with an inflammatory rheumatic disorder.
3. Devise an education plan for the patient with a newly diagnosed inflammatory rheumatic disease.
4. Identify modifications in interventions to accommodate changes in functional ability as the disease progresses.

Key terms: arthritis (inflammation of a joint); exacerbation (symptoms occur or increase); remission (symptoms reduced or absent); pannus (newly formed synovial tissue infiltrated with inflammatory cells); tophi (crystalline deposits in articular surfaces, bone, soft tissue, cartilage); subchondral bone (bony plate supporting articular cartilage); cytokines.

I. Rheumatic Diseases - Overview

• More than 100 types; autoimmune, degenerative, inflammatory, and systemic conditions of joints, muscles, and soft tissue
• Most common features: arthritis and pain
• Women 2 to 9 times more affected than men
• Course: acute or insidious onset, periods of remission and exacerbation; permanent disability possible
• Classification: monoarticular vs polyarticular; inflammatory vs noninflammatory (OA is noninflammatory, covered in Ch. 36)

A. Pathophysiology - three characteristics

1. Inflammation
   • Antigen triggers immune response; immune complexes form; phagocytosis produces leukotrienes (attract more WBCs) and prostaglandins (modify inflammation)
   • Enzymes such as collagenase break down joint collagen leads to edema and synovial proliferation
   • Chronic inflammation leads to pannus formation, then cartilage destruction and bone erosion (Fig. 34-1)
2. Autoimmunity - body recognizes its own tissue as foreign; can involve blood vessels (vasculitis, arteritis), lungs, heart, kidneys; HLA genes linked
3. Degeneration (degradation) - inflammation is secondary; cartilage failure with mechanical stress and bone stiffening

B. Clinical manifestations

• Most common symptom: pain
• Also joint swelling, limited movement, stiffness, weakness, fatigue

C. Assessment (Chart 34-1)

• Health history: onset and evolution of symptoms, family history, patient’s perception, prior treatments, supports
• Physical exam plus functional assessment (what the patient reports and what they demonstrate, such as dressing, rising from a chair); note adaptations (bending to the fork instead of raising it)
• Chart 34-1 highlights:
  • Skin: rash (SLE, vasculitis), photosensitivity (SLE, dermatomyositis), bruising and thinning (medication effect)
  • Hair: alopecia
  • Eyes: dryness, grittiness (Sjogren’s with RA and SLE); decreased acuity (temporal arteritis); cataracts (medication); conjunctivitis, uveitis (ankylosing spondylitis, Reiter’s)
  • Ear: tinnitus, decreased acuity (medication effect, for example salicylates)
  • Mouth: lesions (vasculitis), dryness (Sjogren’s), dysphagia (myositis)
  • Chest: pleuritic pain (RA, SLE); decreased chest expansion (ankylosing spondylitis)
  • Cardiovascular: blanching of fingers in cold (Raynaud’s)
  • Neuro: paresthesias, nerve compression (carpal tunnel); headaches (temporal arteritis)
  • Musculoskeletal: redness, warmth, swelling, tenderness, deformity; first joint involved, pattern, symmetry; muscle atrophy, subcutaneous nodules, popliteal cyst; grip strength decreases with disease activity

D. Laboratory studies (Table 34-1)

• Imaging: x-ray, CT, MRI, arthrography (see Ch. 35)

E. Medical management

• Shared decision-making based on patient values, preferences, comorbidities
• Drug classes: salicylates, NSAIDs, nonbiologic and biologic DMARDs, corticosteroids (Table 34-2; see Medications below)
• DMARDs suppress the autoimmune response, alter disease progression, can induce remission
• Nonpharmacologic pain management:
  • Heat (warm baths, moist compresses, paraffin dips for wrists and small joints); maximum benefit within 20 minutes; more frequent, shorter use is best; exercise is easier after heat
  • Splints rest acutely inflamed joints; canes, crutches, walkers relieve weight-bearing stress; cervical collars; metatarsal bars and shoe pads
• Exercise (Table 34-3):
  • Range of motion - at least daily, active or active-assisted; fewer repetitions when inflamed
  • Isometric - 70% of maximal voluntary contraction daily; monitor BP (isometrics can raise BP)
  • Dynamic - against gravity, add progressive resistance, 2-3 days/week; may stress unstable joints
  • Aerobic - 3-5 days/week, 20-30 minutes moderate intensity; progress slowly
  • Pool - heated pool, deep water to reduce joint compression, nonslip footwear
  • Mild analgesic before exercise may help; report acute or prolonged pain with exercise
  • Weight reduction to relieve stress on painful joints
• Sleep: short-term low-dose antidepressant (amitriptyline); sleep hygiene (set sleep and wake times, quiet room, avoid alcohol and caffeine, get up and read if unable to sleep)
• Activity levels vary day to day with diffuse connective tissue disease (RA, SLE); adjust treatment to disease activity

F. Nursing management (Chart 34-3 plan of care)

• Pain: heat or cold, massage, position changes, foam mattress, splints, relaxation; medications on an individualized schedule; the patient’s description of pain is more reliable than vital signs or facial expression
• Fatigue: fatigue is directly related to disease activity; sleep routine, energy conservation (pacing, delegating, priorities), alternate rest and activity, conditioning program, iron-rich nutrition
• Impaired mobility: PT/OT, ROM, assistive devices, safe footwear, posture; identify environmental barriers; allow ample time and rest after activity
• Self-care deficits: assistive devices, patient controls timing of self-care, energy conservation and work simplification; community referrals
• Disturbed body image and ineffective coping: verbalization, identify past coping, enlist family support
• Medication side effects: periodic clinical and lab monitoring, teaching on self-administration and side effects

G. Gerontologic considerations

• Comorbidities can mask or alter symptoms; rheumatic disease may become a secondary concern
• Decreased vision, hearing, memory, and depression contribute to nonadherence; use memory aids
• Assess pain by behavior (gait, guarding, joint flexion) with cognitive impairment; older men may not report pain unless asked
• Older adults may see symptoms as normal aging and not seek help; may see assistive devices as a sign of aging
• Decreased renal function alters NSAID metabolism; long-term NSAIDs raise risk of peptic ulcer, hemorrhage, cardiovascular toxicity; try acetaminophen first
• Patients may request frequent intra-articular steroid injections without knowing the consequences
• Strength training is encouraged

II. Diffuse Connective Tissue Diseases

Chronic, systemic, diffuse inflammation and degeneration of connective tissue; course of exacerbations and remissions; immunologic cause suspected. Includes RA, SLE, Sjogren’s, scleroderma, polymyositis, PMR, giant cell arteritis.

A. Rheumatoid Arthritis (RA)

Epidemiology and risk:

• Autoimmune; affects 1-2% of the population; women 3 times more than men
• Onset commonly in the third to sixth decades; incidence increases after the sixth decade; onset after 65 is elderly onset RA
• Risks: family history, environment, nulliparity, smoking, obesity (modifiable: smoking and obesity)

Pathophysiology:

• Autoimmune reaction in synovial tissue; synovium breaks down collagen leads to edema, synovial proliferation, pannus
• Pannus destroys cartilage and erodes bone leads to loss of articular surfaces and joint motion
• Muscle degeneration; tendons and ligaments lose elasticity and contractile power
• Linked to arteriosclerosis (interferes with HDL production)
• Synovial inflammation can compress nerves causing neuropathies and paresthesias; vasculitis possible

Diagnostic criteria (ACR/EULAR):

• Point system; score of 6 or greater required for RA
• Based on joint involvement (number of joints), serology (RF or anti-citrullinated peptide antibody, ACPA), acute phase reactants (ESR or CRP), and symptom duration greater than 6 weeks

Clinical manifestations:

• Early: symmetric joint pain and morning stiffness lasting longer than 1 hour
• Classic: symmetric pain, swelling, warmth, erythema, lack of function; joints feel spongy or boggy; fluid can be aspirated
• Pattern starts in small joints of the hands, wrists, feet, then knees, shoulders, hips, elbows, ankles, cervical spine, TMJ
• Onset usually acute; bilateral and symmetric
• Guarding and immobilizing hot, swollen joints leads to contractures
• Deformities: ulnar deviation, swan neck deformity, feet deformities; subluxation (partial dislocation)
• RA deformities differ from OA’s Heberden’s and Bouchard’s nodes
• Extra-articular (most common): fever, weight loss, fatigue, anemia, lymph node enlargement, Raynaud’s phenomenon (cold- and stress-induced vasospasm, digital blanching or cyanosis)
• Rheumatoid nodules: advanced RA, nontender, movable, over bony prominences such as the elbow; only in patients who have rheumatoid factor
• Other: arteritis, neuropathy, pericarditis, splenomegaly, Sjogren’s (dry eyes and mucous membranes)

Assessment and diagnostics:

• RF present in many but not diagnostic alone; absence does not rule out RA
• Anti-CCP: about 95% specificity for RA
• ESR and CRP elevated in acute phases; used to monitor activity and progression
• CBC baseline before medications; anemia; platelets may be elevated
• TB skin test before certain medications (latent TB can reactivate)
• Screen for hepatitis B and C before medications; treat infection first
• Liver and kidney monitoring for most DMARDs
• X-ray and ultrasound of hands, wrists, feet for baseline; joint damage may occur within the first 6-12 months; MRI detects small erosions

Medical management:

• Goals: decrease pain and swelling, achieve remission, decrease deformity, minimize disability; early aggressive treatment (delay leads to more deformity)
• Early RA: start a nonbiologic DMARD (methotrexate preferred; also leflunomide, sulfasalazine, hydroxychloroquine), a biologic, or tofacitinib within 3 months of onset
• Biologic DMARDs target TNF-alpha, B cells, T cells, IL-1, IL-6; work faster and slow radiologic progression more, but cost more; usually reserved for moderate to severe RA not responding to synthetic DMARDs
• Benefit from DMARDs generally within 6 weeks
• Corticosteroids as a “bridge” early, not long term
• JAK inhibitors with methotrexate or alone
• NSAIDs and COX-2 blockers for pain and inflammation only; they do not prevent erosions or alter disease progression
• Opioids avoided
• Established RA: OT/PT for pacing, work simplification, ROM, strengthening; combination therapy (one nonbiologic plus one biologic DMARD) is common
• Surgery when pain cannot be relieved and independence is threatened: synovectomy, tenorrhaphy (tendon suturing), arthrodesis (joint fusion), joint replacement; not done during exacerbations
• Single severely inflamed large joint: local corticosteroid injection
• Topical: capsaicin, methylsalicylate, diclofenac gel
• Low-dose antidepressants (amitriptyline, paroxetine, sertraline) for sleep and depressive symptoms

Obesity considerations:

• About 20% obese at diagnosis; obesity worsens disease progression, function, and quality of life
• Oral corticosteroids stimulate appetite; about half of first-year BMI increase attributed to steroids
• Diet: five food groups; emphasize vitamins, protein, iron for tissue repair; calorie restriction if overweight

Nursing management:

• Most common issues: pain, sleep disturbance, fatigue, altered mood, limited mobility
• Complications: cardiovascular disease is the primary cause of death in up to 40% of RA patients (lipids, chronic inflammation, endothelial dysfunction, homocysteine)
• Monitor for medication adverse effects; medication may need to be stopped or reduced
• Teaching (Chart 34-4 Home Care Checklist): medications (name, dose, side effects, schedule), safe self-administration, pain management techniques, ADLs with assistive devices, exercise, rest, stress management, diet, follow-up, community resources
• Topical analgesics: apply sparingly, avoid open skin, eyes, mucous membranes; wash hands after; check for skin irritation
• Address pain, fatigue, depression before teaching
• Acupuncture is safe and may help; other complementary therapies need more research
• Young women: concerns about childbearing, family care, work
• Home care: assess safety and adherence; for example a patient with diabetes may be unable to fill an insulin syringe due to joint limitation; referrals to PT/OT, Meals on Wheels, Arthritis Foundation
• Patients should know which rheumatic disease they have, not just “arthritis”

B. Systemic Lupus Erythematosus (SLE)

Epidemiology:

• Inflammatory, autoimmune; affects nearly every organ
• Incidence 1.8-7.6 per 100,000
• 4 to 12 times more common in women
• More common in African Americans, Hispanic/Latino Americans, Asians, American Indians/Alaska Natives than White Americans
• Other forms: subacute cutaneous or discoid lupus, drug-induced lupus

Pathophysiology:

• Immune system sees components of the cell nucleus as foreign; B cells overproduce antibodies, helped by B-lymphocyte stimulator (BLyS)
• Antigen-antibody complexes trapped in capillaries of visceral structures; antibodies also destroy host cells
• Factors: genetic, immunologic, hormonal (estrogen), environmental
• Triggers: cigarette smoke, UV rays (sunlight, fluorescent light), medications (hydralazine, minocycline, procainamide), viral infections, emotional stress, physical stress (surgery, pregnancy), silica dust

Clinical manifestations (Fig. 34-2):

• Chronic periods of minimal symptoms alternating with acute flares
• Most common: fever, fatigue, skin rash, joint pain and swelling
• Systems most involved: mucocutaneous, musculoskeletal, renal, nervous, cardiovascular, respiratory
• Skin (up to 85%): butterfly rash, subacute cutaneous lesions, discoid rash (scarring, pigment changes); worsened by sunlight or artificial UV light
• Oral ulcers (buccal mucosa, hard palate) in crops, with exacerbations
• Other skin: splinter hemorrhages, alopecia, Raynaud’s
• Joints: pain and swelling in more than 90%; morning stiffness; symmetric like RA
• Cardiac: pericarditis is the most common cardiac manifestation (substernal chest pain worse with movement or inspiration); also myocarditis, hypertension, arrhythmias, valve incompetence
• Renal: lupus nephritis from immune complex damage to nephrons; screen with serum creatinine and urinalysis; can lead to hypertension
• CNS: psychosis, cognitive impairment, seizures, neuropathies, transverse myelitis, stroke; often subtle behavior or cognitive changes
• Hematologic: anemia, neutropenia, thrombocytopenia

Assessment and diagnostics:

• Skin: erythematous rashes, plaques with adherent scale on scalp, face, neck; hyper- or depigmentation; ask about sun sensitivity
• Scalp for alopecia; mouth and throat for ulcers
• Auscultate for pericardial friction rub and abnormal lung sounds (pleural effusion)
• Papular, purpuric lesions on fingertips, elbows, toes that may become necrotic suggest vascular involvement
• Neuro and behavior changes, depression, seizures, chorea
• ANA positive in more than 95%
• Anti-DNA; anti-ds DNA (highly specific to SLE, differentiates from drug-induced lupus); anti-Sm (specific)
• CBC: anemia, thrombocytopenia, leukocytosis, or leukopenia

Medical management:

• Goals: prevent progressive organ loss, reduce acute disease, minimize disability, prevent treatment complications
• Belimumab: monoclonal antibody that binds BLyS and halts unnecessary antibody production; no live vaccines for 30 days before
• Rituximab: additional monoclonal antibody
• Corticosteroids: topical for skin, low oral dose for minor activity, high dose for major activity, IV alternative; major risk is osteoporosis and fractures
• Hydroxychloroquine: cutaneous, musculoskeletal, mild systemic features
• NSAIDs with corticosteroids to minimize steroid dose
• Immunosuppressives (cyclophosphamide, azathioprine, mycophenolic acid, methotrexate) for serious disease, especially lupus nephritis; contraindicated in pregnancy

Nursing management:

• Common diagnoses: fatigue, impaired skin integrity, body image disturbance, knowledge deficit
• Avoid sun and UV exposure; sunscreen and protective clothing
• Routine screenings; diet consult for cardiovascular risk (hypertension, atherosclerosis)
• Smoking and vaping cessation (higher lung cancer risk; smoking can impair hydroxychloroquine)
• Watch for infection with systemic corticosteroids
• Osteoporosis screening: bone mineral density at diagnosis and before steroids, then every 2 years; calcium, vitamin D, weight-bearing activity

C. Primary Sjogren’s Syndrome

• Rare systemic autoimmune disease, mostly middle-aged women; often with autoimmune thyroid disease, RA, SLE
• Lymphocytic infiltration leads to failure of lacrimal and salivary glands
• Symptoms: keratoconjunctivitis sicca (dry, “gritty” eyes), xerostomia (dry mouth, difficulty swallowing), pain, fatigue; Raynaud’s; neuropathies; depression, anxiety, sleep disturbance
• Diagnostics: Schirmer tear test, Rose Bengal; salivary gland biopsy; anti-Ro (SS-A) and anti-La (SS-B); RF in 50-70%
• Treatment: no cure; artificial tears, pilocarpine, topical cyclosporine, punctum plugs; pilocarpine increases salivary flow; Biotene rinse; small frequent meals, avoid spicy and salty foods, smoking, alcohol, anticholinergic drugs
• Nursing: teach eye care to avoid eye infections; screen for depression and sleep problems

D. Scleroderma

• Rare autoimmune disease of skin, blood vessel walls, internal organs; localized (skin only) or diffuse (systemic sclerosis)
• Women 4 times more than men; onset 25-50 years
• Excess collagen accumulates; edema leads to taut, shiny skin, then fibrosis and loss of elasticity
• Skin cannot be pinched up; masklike “stone facies”; extremities stiffen
• Internal: esophagus hardens (dysphagia), lungs scar, GI sclerosis, renal vascular involvement leads to malignant hypertension and renal insufficiency; pericarditis, heart block, myocardial fibrosis
• CREST: Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia; diagnosis if 4 of 5
• Treatment symptomatic; ACE inhibitors for kidney involvement have greatly reduced mortality from hypertensive kidney disease
• Moderate exercise to prevent contractures; avoid extreme temperatures; lotion for dry skin
• Nursing: meticulous skin care and preventing effects of Raynaud’s are major challenges

E. Polymyositis

• Idiopathic inflammatory myopathy; women 2:1; age 40-50
• Slow onset; symmetric proximal muscle weakness is the first symptom (difficulty rising from chair, climbing stairs, holding up head, combing hair)
• Dermatomyositis: erythematous lesion over joints, often before weakness
• Diagnostics: EMG, muscle biopsy, increased serum muscle enzymes
• Corticosteroids are the mainstay; IVIG, plasmapheresis if no response; hydroxychloroquine for rash; slow PT (ROM then strengthening)

F. Polymyalgia Rheumatica (PMR) and Giant Cell Arteritis (GCA)

• One disease spectrum; over age 50; mostly Caucasians; PMR 2-3 times more common than GCA
• PMR: severe aching and stiffness of neck, shoulder, pelvic girdle; worse in morning and after inactivity; low-grade fever, weight loss, malaise, depression; may be dismissed as aging
• GCA (temporal arteritis): headache, vision changes, jaw claudication; evaluate immediately - risk of blindness and stroke
• Diagnostics: markedly high ESR (screen); ESR plus CRP elevation 98.6% sensitive for GCA; temporal artery biopsy is definitive; dramatic response to corticosteroids
• Treatment: PMR moderate-dose corticosteroids with gradual taper; GCA rapid start and strict adherence to corticosteroids to prevent blindness; aspirin adjunct
• Nursing: patients may stop steroids when symptoms improve - stopping must follow the prescription; Quality and Safety Nursing Alert: emphasize adherence to prevent blindness and stroke; bone health (calcium, vitamin D, BMD, weight-bearing exercise)

III. Spondyloarthropathies

• Ankylosing spondylitis (AS), reactive arthritis (Reiter’s), psoriatic arthritis; associated with Crohn’s and ulcerative colitis
• Inflammation at sites of attachment (tendons, joint capsules, ligaments); sacroiliac arthritis common; young adult men; familial; HLA-B27 often present
• Increased cardiovascular risk
• AS: chronic inflammation of the spine; males, second or third decade; back pain is characteristic and can mask a cervical fracture; kyphosis; heart and lungs constricted; complications include osteoporosis, AV conduction defects, aortic insufficiency, pulmonary fibrosis; full spine ankylosis can compromise respiration
• Reactive arthritis: follows GI or GU infection; young men; urethritis, arthritis, conjunctivitis; mouth and penile ulcers; low back pain
• Psoriatic arthritis: about 7% of people with psoriasis; onset 30-50, men and women equally; synovitis, polyarthritis, spondylitis; inflammatory back pain (young onset, improves with activity, at night); asymmetric sacroiliitis; enthesis pain (Achilles, plantar fascia, tibial tuberosity)
• Management: NSAIDs first-line for all spondyloarthropathies; methotrexate, sulfasalazine, leflunomide for skin and peripheral joints; corticosteroid injections for flares; avoid long-term oral steroids (psoriatic skin flare on withdrawal); anti-TNF agents; apremilast; ustekinumab
• AS: good posture and positioning so that if ankylosis occurs, it is in the most functional position; ROM and strengthening
• Surgery: spinal osteotomy for kyphosis; joint replacement
• Nursing: young men concerned about prognosis and job; stay active, maintain posture; address depression

IV. Metabolic and Endocrine Diseases Associated With Rheumatic Disorders

Most common: crystal-induced arthropathies - monosodium urate (gout) and calcium pyrophosphate (pseudogout).

A. Gout

Epidemiology:

• Most common form of inflammatory arthritis; more than 8.3 million Americans; prevalence about 3.9% and rising
• Men 3-4 times more likely
• Risk rises with age, BMI, alcohol, hypertension, diuretic use, fructose-rich beverages
• Increased cardiovascular risk; comorbid hypertension, dyslipidemia, diabetes, OA, kidney disease, depression

Pathophysiology:

• Caused by hyperuricemia; uric acid is a by-product of purine metabolism (purines high in meat)
• Hyperuricemia defined as serum urate greater than 6.8 mg/dL; does not always cause crystal deposition, but risk rises with level
• Macrophages phagocytize urate crystals; IL-1 beta secreted; worsened by free fatty acids (alcohol, large meals with red meat are triggers)
• Repeated attacks lead to tophi in the great toe, hands, ear; renal urate stones and chronic kidney disease
• Primary hyperuricemia: severe dieting or starvation, high-purine foods (shellfish, organ meats), heredity
• Secondary hyperuricemia: increased cell turnover (leukemia, multiple myeloma, some anemias, psoriasis); uric acid underexcretion from thiazides, furosemide, low-dose salicylates, ethanol

Clinical manifestations:

• Acute gouty arthritis, tophi, gouty nephropathy, uric acid urinary calculi
• Four stages: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, chronic tophaceous gout
• Lifelong urate-lowering therapy deferred until the first attack
• Acute attack: metatarsophalangeal joint of the big toe most common; also tarsal area, ankle, knee
• Triggers: trauma, alcohol, dieting, medications, surgical stress, illness
• Abrupt onset, often at night, with severe pain, redness, swelling, warmth
• Early attacks resolve in 3-10 days without treatment; symptom-free intercritical period may last months to years; over time attacks become more frequent, involve more joints, last longer
• Tophi: with more frequent and severe attacks and higher urate levels; in synovium, olecranon bursa, subchondral bone, tendons, subcutaneous tissue; also heart valves, ear cartilage, eyelids

Diagnosis:

• Definitive: polarized light microscopy of synovial fluid shows uric acid crystals within polymorphonuclear leukocytes
• Serum uric acid may be normal during an acute flare

Medical management:

• Acute attack: colchicine (oral or parenteral), an NSAID such as indomethacin, or a corticosteroid; treat early
• After the acute attack subsides: urate-lowering therapy; xanthine oxidase inhibitors (allopurinol, febuxostat) are the agents of choice
• Uricosuric (probenecid) for frequent attacks
• Pegloticase for refractory chronic gout
• Anakinra (IL-1 antagonist) may have a role in acute gout
• Treatment based on serum urate, 24-hour urine uric acid, renal function

Nursing management:

• Use both written and verbal teaching; providers overestimate patient knowledge
• Severe dietary restriction not needed; limit high-purine foods (especially organ meats) and alcohol; maintain normal weight
• Acute attack: medications for pain; avoid trauma, stress, alcohol
• Adherence to urate-lowering therapy is poor; patients feel well between attacks and stop medications, leading to another attack

V. Fibromyalgia

• Chronic pain syndrome: fatigue, generalized muscle aching, stiffness, sleep disturbance, functional impairment
• More than 5 million Americans (2-5%); women more than men; 25-65% have another rheumatic condition
• Neurogenic: abnormal CNS pain processing amplifies pain (“volume control set too high”); touch may cause pain
• Predisposing: anxiety, depression, trauma, emotional stress, sleep disorder, viral infection
• Diagnosis: tests mostly rule out other causes; screening items - pain on pinching the Achilles tendon (4 kg for 4 seconds) and “I have a persistent deep aching all over my body”
• Treatment: NSAIDs; tricyclics (amitriptyline, nortriptyline) and sleep hygiene; cyclobenzaprine; CBT; SNRIs (duloxetine, venlafaxine, milnacipran); SSRIs; gabapentin, pregabalin; individualized exercise; acupuncture promising
• Nursing: patients may feel not taken seriously; listen carefully, support, support groups

VI. Miscellaneous Disorders

Trauma (internal derangement, loose bodies), pancreatic disease (avascular necrosis), sarcoidosis, palindromic rheumatism, villonodular synovitis, chronic active hepatitis, drug-related rheumatic syndromes.

Lecture vs Textbook Differences

The Oct 14 lecture deck (nsg210-week-08-rheumatic-diseases-lecture) differs from this chapter in a few places. Learn the slide values for the exam unless the instructor says otherwise.

High-Yield Numbers

• RA: 1-2% of population; women 3:1; diagnostic score 6 or greater; symptoms more than 6 weeks; morning stiffness longer than 1 hour; RF in 80%; anti-CCP about 95% specific; DMARD within 3 months of onset; benefit within about 6 weeks; joint damage within first 6-12 months; CVD causes death in up to 40%
• SLE: women 4-12 times more; ANA positive in more than 95%; skin involvement up to 85%; joint involvement more than 90%; BMD every 2 years on steroids; no live vaccines 30 days before belimumab
• Gout: hyperuricemia over 6.8 mg/dL; men 3-4 times more; untreated early attacks last 3-10 days
• ESR normals: men under 50, under 15 mm/h; women under 50, under 20; women over 50, under 30
• RF positive titer over 1:80; HLA-B27 in 80-90% of AS
• Heat: maximum benefit within 20 minutes
• Aerobic exercise: 3-5 days/week, 20-30 minutes; isometric at 70% maximal contraction
• Hydroxychloroquine: eye exam every 6-12 months; onset 2-4 months
• Methotrexate labs: CBC, liver enzymes, creatinine at 6 weeks, then every 2-3 months
• Cyclosporine: BP and creatinine every 2 weeks until stable
• GCA: ESR plus CRP 98.6% sensitive
• Scleroderma: CREST diagnosis with 4 of 5

Priority Nursing Actions and Red Flags

• Test for TB (and hepatitis B and C) before biologic DMARDs, JAK inhibitors, and other immunosuppressants
• Biologics: hold the dose and notify the provider if fever or infection occurs
• GCA: new headache, vision changes, or jaw claudication need immediate evaluation (blindness, stroke); stress steroid adherence
• SLE: watch for pericarditis (chest pain worse with inspiration, friction rub), rising creatinine or abnormal urinalysis (lupus nephritis), neuro or behavior changes, infection on steroids
• RA: assess for cardiovascular disease, the leading cause of death
• AS: severe back pain can mask cervical fracture
• Gout: do not start or increase allopurinol or febuxostat during an active flare; colchicine - stop when pain is relieved or diarrhea develops
• Methotrexate, leflunomide, cyclophosphamide, azathioprine: teratogenic; teach contraception
• Steroids: osteoporosis and fracture risk, hyperglycemia (caution in diabetes), infection
• Older adults: NSAID GI bleed and renal risk; consider acetaminophen first
• Surgery for RA is not done during an exacerbation

Medications

Related

• nsg210-hinkle-ch36-musculoskeletal-disorders - osteoarthritis and joint replacement (same lecture)
• INDEX - NSG210 chapter index
• nsg210-textbook-chapter-crosswalk