NSG210 Week 08 Lecture: Alterations in Activity and Rest - Inflammatory Rheumatic Diseases

Course: NSG210 Medical-Surgical Nursing, Fall 2026 Week: 08 (Oct 12-16), lecture Oct 14 Exam: Exam 3

Source: lecture deck raw/nsg210_AlterationActivityRestRheumaticDiseases2026.pptm (56 slides; text extract raw/nsg210_AlterationActivityRestRheumaticDiseases2026.md). Topics: rheumatoid arthritis, lupus, gout, plus joint replacement. Slides 5, 23, 25, and 49 are images (pannus formation, RA of the hand, RA joint deformities, classic gout). Slides 37-45 and 51-56 are unfolding case studies with NCLEX-style questions; answers and rationales below are worked out from the slides and textbook (the deck does not include an answer key). Where the slides differ from the textbook, the slide value is given with the textbook value noted.

Textbook: Hinkle Ch. 34 nsg210-hinkle-ch34-inflammatory-rheumatic-disorders (RA, SLE, gout) and Ch. 36 nsg210-hinkle-ch36-musculoskeletal-disorders (joint replacement).

Learning Outcomes (slide 2)

1. Explain the pathophysiology of inflammatory rheumatic diseases and their assessment and diagnostic findings.
2. Use the nursing process for the patient with an inflammatory rheumatic disorder.
3. Devise an education plan for a patient newly diagnosed with an inflammatory rheumatic disease.
4. Modify interventions as functional ability changes with disease progression.

I. Rheumatic Diseases Overview (slides 3-9)

• “Arthritis” / rheumatic disease affects skeletal muscle, bone, cartilage, ligaments, tendons, joints
• Course of remission and exacerbation
• Three hallmark processes:
  • Inflammation: immune response to antigens; antibodies and immune complexes deposit in synovium or organs, causing effusion, pain, and edema; PANNUS (inflamed granulation tissue) forms and destroys cartilage and bone
  • Autoimmunity: body treats its own tissue as foreign, leading to inflammatory destruction
  • Degeneration: genetics, hormones, mechanical stress, prior injury cause cartilage failure and stiff bone ends; inflammation is secondary (this is osteoarthritis)
• Local manifestations: pain, joint swelling, limited movement, stiffness, weakness, fatigue
• Systemic effects: fever, fatigue, anemia, enlarged lymph nodes, Raynaud phenomenon, Sjogren syndrome; any organ - arteritis, neuropathy, scleritis, pericarditis, pleural effusion, splenomegaly, kidney involvement; skin and mucosal lesions
• Assessment: health history, functional assessment, arthrocentesis (aseptic needle aspiration of synovial fluid), x-ray, bone scan, CT, MRI, arthroscopy, tissue biopsy
• Labs (assume autoimmune; does not apply to OA; NO single test confirms diagnosis): ESR, ANA, rheumatoid factor, uric acid; also creatinine, hematocrit, WBC

II. Medical Management Goals (slide 10)

• Interdisciplinary program that fits the patient’s lifestyle
• Suppress inflammation and autoimmune response; control pain; maintain or improve joint mobility and function; increase knowledge; promote self-management

III. Pharmacologic Therapy (slides 11-16)

IV. Nonpharmacologic Pain Management and Nursing Problems (slides 17-18)

• Heat and cold; assistive devices; individualized exercise (passive, assistive, active ROM; strengthening; aerobic); mild analgesic BEFORE activity
• Sleep: short-term low-dose amitriptyline to restore sleep and improve pain; sleep routine
• Problems: acute and chronic pain, fatigue, disturbed sleep, impaired mobility, self-care deficits, disturbed body image, ineffective coping; monitor for complications

V. Gerontologic Considerations (slide 19)

• Arthritis is NOT an inevitable part of aging (myth)
• Other conditions can hide or outrank the diagnosis; OA more common with age
• Osteoporosis risk higher with diffuse connective tissue disease
• Threatens independence; risk of over- or inappropriate treatment; drugs harder to use (altered metabolism, more side effects)

VI. Home and Community Care and Teaching (slides 20-21)

• Self-care: maximum independence, safe medication use, proper use of assistive devices
• Continuing care: home safety, adherence, skin checks and prevention, reinforce teaching
• Teaching content: disease and management principles, medications, monitoring, information sources, pain management, JOINT PROTECTION, assistive devices, exercise and relaxation

VII. Rheumatoid Arthritis (slides 22-27)

• Systemic autoimmune disease with chronic inflammation of joints, surrounding tissue, and other organs; progressive; can destroy connective tissue and cause disability
• Manifestations:
  • Joint pain, swelling, warmth, erythema, loss of function
  • MORNING STIFFNESS lasting MORE THAN 1 HOUR
  • Spongy, soft joints on palpation
  • Small joints first, then larger; BILATERAL and SYMMETRIC; acute onset
  • Hand and foot deformities; nontender, movable rheumatoid nodules
  • Extra-articular: fever, weight loss, fatigue, anemia, enlarged nodes, Raynaud; vasculitis, pericarditis, pleuritis; Sjogren (dry eyes and mouth)
• Diagnostics:
  • Rheumatoid factor in 80%
  • ACPA (anti-CCP) detects RA earlier, 95% specificity
  • Elevated ESR
  • Decreased RBCs and C4 complement
  • Synovial fluid cloudy, milky, or dark yellow
  • X-ray: bony erosions and narrowed joint spaces (late)
• Management goals: decrease pain and swelling; achieve clinical remission; prevent deformity; minimize disability; EARLY and AGGRESSIVE treatment; monitor drug complications

VIII. Joint Replacement (slides 28-30)

• Types: total hip (THA - femoral head and acetabulum replaced), total knee (TKA - femur, tibia, sometimes patella), shoulder, partial replacement, revision (redo for loosening, wear, infection, failure)
• Indications: persistent pain, impaired mobility, decreased ADLs when conservative treatment fails; OA, RA, severe degeneration, trauma or fracture, avascular necrosis (especially hip), loss of function
• Pre-op nursing: establish baseline, identify risks, physical and psychological preparation, promote recovery
• Post-op nursing: prevent complications (see Ch. 36 outline for hip precautions, dislocation, VTE, infection, neurovascular checks)

IX. Systemic Lupus Erythematosus (slides 31-36)

• Inflammatory autoimmune disease that can cause major organ failure
• Other forms: discoid, drug-induced, neonatal
• Triggers: genetic, hormonal (onset in childbearing years), environmental (sunlight, UV); drugs - isoniazid, hydralazine, antiseizure medications
• Skin: discoid rash (red scaly papules on scalp, face, neck); BUTTERFLY (malar) rash over cheeks and nose; provoked by sun or UV light; oral ulcers; Raynaud
• Systemic: arthralgia and arthritis (synovitis), extreme fatigue, pericarditis, atherosclerosis risk in women, CNS (depression, trouble thinking, memory problems), NEPHRITIS and kidney disease, unexplained fever, sun sensitivity, low blood counts
• Classification (ACR, per slides): diagnosis if 4 of 11 criteria - malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, kidney disease, neurologic disease, hematologic disorder, immunologic disorder, positive ANA
• Medical management: control exacerbations; prevent loss of organ function; reduce acute flares
  • NSAIDs, corticosteroids, antimalarials (hydroxychloroquine); immunosuppressants only if no response to conservative therapy
  • Belimumab (Benlysta): decreases unnecessary antibody production and disease activity
• Nursing: rheumatic disease diagnoses; support groups; AVOID SUNLIGHT and UV light (sunscreen, protective clothing); diet HIGH in vitamins and IRON; watch for bruising, bleeding, injury; meds as prescribed; periodic screenings

X. Case Study: SLE - Maria R., 29 (slides 37-45)

Scenario: SLE for 4 years with suspected lupus nephritis; increasing fatigue, joint pain, facial swelling, decreasing urine output for a week; STOPPED her corticosteroid because she “feels better”; hours outdoors without sunscreen.

Findings: T 100 F, HR 96, RR 20, BP 158/94, SpO2 97%; weight up 4 kg (68 to 72 kg); periorbital and bilateral ankle edema; butterfly rash; hand and knee pain and stiffness; fatigue 8/10; foamy urine; urine output 25 mL/hr.

Labs: creatinine 2.1 (high), BUN 34 (high), urinalysis protein 3+ and blood 2+, Hgb 10.2 (low), WBC 3,200 (low), platelets 155,000 (near normal), ANA positive, anti-dsDNA elevated (SLE activity).

Interpretation: lupus nephritis flare - proteinuria (foamy urine), hematuria, oliguria (under 30 mL/hr), rising creatinine and BUN, fluid retention (weight gain, edema, HTN); triggered by stopping steroids and sun exposure; anemia and leukopenia are hematologic SLE features.

XI. Gout (slides 46-50)

• Inflammatory arthritis from too much uric acid; urate crystals deposit in joints and tissues
• Uric acid over 7 mg/dL (slide; textbook defines hyperuricemia as over 6.8 mg/dL) with recurrent joint inflammation
• Causes: faulty purine metabolism, decreased renal excretion, severe dieting or starvation, high-purine foods (SHELLFISH, ORGAN MEATS), heredity, ALCOHOL, medications such as DIURETICS
• Attacks follow sudden RISES or FALLS in uric acid as crystals precipitate in a joint
• Tophi (sodium urate deposits) in great toe, hands, elbows; kidney deposits form urate stones and can cause kidney failure
• Manifestations: excruciating pain, swelling, inflammation (BIG TOE usually first); tophi may drain a yellow gritty substance; low-grade fever, malaise, headache, pruritus, kidney stones; elevated uric acid, WBC, ESR
• Management:
  • LOW-PURINE diet, NO alcohol; bed rest during acute attacks
  • Colchicine: ACUTE attacks; lowers urate deposition and inflammation; GI upset (diarrhea); long-term use lowers vitamin B12 absorption
  • Probenecid: uricosuric (blocks renal reabsorption, increases urinary excretion); nausea, rash, constipation
  • Allopurinol: LONG-TERM maintenance; blocks purine breakdown before uric acid forms; watch for bone marrow depression, vomiting, abdominal pain
  • Corticosteroids (may be intra-articular); NSAIDs for pain, swelling, stiffness
  • (Textbook adds: fluids 2-3 L/day to prevent stones; do not start allopurinol during an acute attack)

XII. Case Study: Gout - Robert M., 58 (slides 51-56)

Scenario: HTN, CKD stage 2, obesity, recurrent gout; takes HYDROCHLOROTHIAZIDE (thiazide raises uric acid) and lisinopril. Sudden severe right great toe pain overnight, 9/10; “even the bedsheet touching my toe hurts.”

Findings: great toe swollen, red, warm, very tender; trouble walking; T 100 F, HR 96, BP 148/88, weight 102 kg. Labs: uric acid 9.8 (high), WBC 11,800 (mildly high), creatinine 1.3, BUN 25, eGFR 64, CRP elevated.

Q1 (multiple response) - findings that support an acute gout flare:

• A sudden onset of severe joint pain - YES
• B warmth and erythema of the joint - YES
• C needle-shaped, negatively birefringent crystals in synovial fluid - YES (the diagnostic finding for gout; note Robert’s results do not list a joint aspiration, so if the question is limited strictly to his reported findings, C would not be selected)
• D serum uric acid 9.8 - YES
• E bilateral painless ankle swelling - NO (gout is acute, painful, usually one joint)
• F severe tenderness to light touch - YES

Q2 (matrix) - acute gout vs consider an alternative or complication:

Q3 (bow-tie) - after colchicine, pain down to 5/10 but profuse watery diarrhea, cramping, nausea, vomiting:

• Most likely problem: B - possible colchicine toxicity/adverse effect
• Priority action: C - hold further colchicine and notify the provider
• Supporting finding: B - profuse diarrhea and vomiting

Teaching points from the case: thiazide diuretics raise uric acid (discuss alternatives with provider); CKD reduces uric acid excretion and affects colchicine dosing; weight loss, low-purine diet, no alcohol, fluids; allopurinol for long-term prevention once the acute attack resolves.

Slide vs Textbook Differences

Likely Exam Points From This Lecture

• Pannus = inflamed tissue that destroys joints in RA
• RA: symmetric, small joints first, morning stiffness over 1 hour, spongy joints, nodules, systemic signs; RF and anti-CCP
• NSAIDs: with food, GI bleeding, raise BP and fluid retention; COX-2 inhibitors raise MI and stroke risk; aspirin toxicity = tinnitus
• Hydroxychloroquine: eye exams; takes 2-4 months
• Methotrexate: teratogenic, CBC and liver tests
• TNF blockers: TB test first, infection risk, subcut teaching
• Steroids: lowest dose shortest time; cataracts, hyperglycemia, HTN, GI; never stop abruptly
• SLE: butterfly rash, photosensitivity, nephritis (watch urine output, creatinine, weight, BP), avoid sun, high iron and vitamin diet, bleeding precautions; infection risk with leukopenia
• Gout: big toe, uric acid, tophi; low-purine diet, no alcohol; colchicine (acute; diarrhea = toxicity), allopurinol (long term), probenecid (excretion); thiazides raise uric acid
• Joint replacement types and indications

Related

• nsg210-hinkle-ch34-inflammatory-rheumatic-disorders
• nsg210-hinkle-ch36-musculoskeletal-disorders - OA and arthroplasty care
• nsg210-week-08-peripheral-vascular-diseases-lecture - same week
• nsg210-week-08-summary - Week 08 hub
• INDEX