RA, HIV/AIDS, Hypersensitivity, Lupus

Hypersensitivity Reactions

• An exaggerated or inappropriate immune response causes tissue damage by reacting to foreign antigens or the body’s own tissues; autoimmune disease occurs when the body fails to recognize self-proteins. Types I, II, and III are immediate and involve humoral immunity, while Type IV is delayed and involves cell-mediated immunity.

Type I: IgE-Mediated Reactions

• First exposure causes the body to produce IgE antibodies, which attach to mast cells and basophils; on later exposure, the allergen binds to IgE and triggers degranulation with release of histamine, leukotrienes, and other mediators.

• These mediators cause smooth muscle contraction, vasodilation, increased vascular permeability, hypotension, increased mucus secretion, and itching. Reactions are immediate (minutes to hours) and do not involve complement.

• Localized reactions can cause a wheal-and-flare response, while systemic reactions can cause anaphylaxis/anaphylactic shock. Other examples include allergic rhinitis, angioedema, asthma, atopic dermatitis, and hives.

Anaphylaxis

• A rapid, life-threatening systemic allergic reaction can occur within minutes after exposure, causing bronchoconstriction, airway obstruction, angioedema, and vascular collapse. Early findings can include itching and edema, followed by wheezing/stridor, dyspnea, hypotension, tachycardia, weak pulse, cyanosis, and shock.

• Other manifestations can include urticaria, dizziness, feeling of impending doom, nausea, vomiting, abdominal cramping, and diarrhea. Without immediate emergency treatment, respiratory or cardiac arrest and death can occur; drugs are the leading cause of anaphylaxis-related deaths.

Atopic Reactions

• An inherited tendency to become sensitive to environmental allergens occurs in about 20% of the population and can lead to allergic rhinitis, asthma, atopic dermatitis, hives, and angioedema.

• Allergic rhinitis is the most common Type I reaction and causes sneezing, nasal drainage, tearing, mucosal swelling, and itching; seasonal cases are commonly triggered by pollens, while perennial cases are commonly triggered by dust, molds, and animal dander. Allergic asthma causes bronchoconstriction, thick mucus, and bronchial edema, producing wheezing, dyspnea, cough, and chest tightness.

• Hives are superficial, transient, pink raised itchy wheals caused by histamine, while angioedema involves deeper skin/submucosal tissues and commonly affects the eyelids, lips, tongue, and larynx; airway involvement can become dangerous. Atopic dermatitis is a chronic inherited disorder with exacerbations/remissions and generalized itchy skin lesions.

Type II: Cytotoxic and Cytolytic Reactions

• IgG or IgM antibodies bind directly to antigens on cell surfaces, activating complement and causing rapid destruction through cell lysis or increased phagocytosis. Common targets include RBCs, platelets, and WBCs.

• Common examples include ABO/Rh transfusion reactions, hemolytic anemia, leukopenia, thrombocytopenia, erythroblastosis fetalis (hemolytic disease of the newborn), and Goodpasture syndrome.

Hemolytic Transfusion Reactions

• ABO-incompatible blood causes recipient antibodies to bind donor RBCs, producing rapid agglutination and complement-mediated hemolysis. Clumped cells can block small vessels and consume clotting factors, causing bleeding, while released hemoglobin enters the blood and urine and can lead to acute kidney injury.

• Remember ABO antibodies: Type A → anti-B, Type B → anti-A, Type AB → no anti-A/anti-B, Type O → anti-A and anti-B.

Goodpasture Syndrome

• An autoimmune Type II hypersensitivity reaction targets the glomerular and alveolar basement membranes; circulating antibodies activate complement and cause IgG deposits in the kidneys and lungs, which can lead to glomerulonephritis and pulmonary hemorrhage.

Type III: Immune-Complex Reactions

• IgG or IgM bind soluble antigens to form immune complexes that are not effectively cleared, so they deposit in small blood vessels or tissues and activate complement, causing inflammation and tissue damage.

• Common deposition sites are the kidneys, skin, joints, blood vessels, and lungs. Major examples include SLE, acute glomerulonephritis, and rheumatoid arthritis.

Type IV: Delayed Hypersensitivity Reactions

• A cell-mediated reaction driven by sensitized T cells, not antibodies or complement, causes tissue damage by releasing cytokines that recruit macrophages; macrophages and their enzymes cause most of the destruction. The response typically appears 24–48 hours after exposure.

• Common examples include contact dermatitis, reactions to bacterial/fungal/viral infections, transplant rejection, and some drug reactions.

Contact Dermatitis

• A Type IV delayed hypersensitivity reaction occurs after skin exposure to an allergen; initial sensitization takes about 7–14 days, and later exposure causes lesions within about 48 hours.

• Acute findings include redness, swelling, itching, papules, vesicles, and bullae; chronic cases become thickened, scaly, and lichenified. Common triggers include nickel, rubber, poison ivy/oak/sumac, cosmetics, and dyes.

• Unlike atopic dermatitis, the rash is usually localized to the area that contacted the allergen, whereas atopic dermatitis is generally more widespread.

Microbial Hypersensitivity Reactions

• A Type IV cell-mediated response occurs when microbial antigens activate T cells, causing inflammation and tissue damage; in tuberculosis, the immune response—not the tubercle bacillus itself—causes caseous necrosis of lung tissue.

• Memory T cells cause a delayed response with later exposure, which is the basis of the PPD tuberculosis skin test; the test is read 48–72 hours after intradermal injection.

Allergic Disorders: Assessment

• Obtain a complete allergy history, including symptoms/severity, age of onset, timing after exposure, duration/frequency, seasonal patterns, previous treatments, family history of allergies/atopy, medication reactions, food intolerances, insect reactions, pets, and environmental exposures.

• Focus the physical assessment on common manifestations: conjunctivitis/tearing, allergic shiners, pale boggy nasal mucosa, sneezing/rhinitis, allergic salute, swollen lips/tongue, wheezing/stridor, thick sputum, hives, wheal-and-flare reactions, and other skin lesions.

• Diagnostic findings may include eosinophilia, increased serum IgE, positive skin tests, and abnormal chest/sinus x-rays. Document all known allergies on the chart, nursing care plan, and medication record.

Allergic Disorders: Diagnostic Studies & Skin Testing

• Key diagnostic findings include CBC with differential, absolute lymphocyte count, eosinophils, and serum IgE. Lymphocytes <1,200/µL suggest immunodeficiency, while elevated eosinophils and IgE are associated with Type I hypersensitivity/atopic disease; pulmonary function testing is useful for asthma.

• Specific allergens can be identified with scratch/prick, intradermal, or patch testing. Scratch/prick and intradermal reactions occur in about 5–10 minutes and produce a positive wheal-and-flare response; patch tests remain in place for 48–72 hours. Blood allergy testing is used when skin testing cannot be done, such as when medications suppress histamine or severe skin disease is present.

• Never leave the patient during skin testing because a highly sensitive patient can develop anaphylaxis. Positive testing means the patient is sensitized, not necessarily that the allergen caused the symptoms, so results must be correlated with the history; false-positive and false-negative results can occur.

Interprofessional and Nursing Management: Anaphylaxis

• Management depends on rapid recognition, maintaining a patent airway, giving emergency medications, and treating shock. Epinephrine is the drug of choice, with high-flow oxygen, IV access, and close monitoring of vital signs, respiratory status, oxygen saturation, level of consciousness, heart rhythm, and urine output.

• For bronchospasm, albuterol may be added; diphenhydramine treats hives/itching, and corticosteroids may be given. If hypotension develops, place the patient recumbent with legs elevated and give a rapid IV normal saline bolus; severe airway edema may require intubation, cricothyrotomy, or tracheostomy.

• Patients taking β-blockers may respond poorly to epinephrine and can develop refractory hypotension/bradycardia; glucagon is used because its effects do not depend on β-receptors.

Interprofessional and Nursing Management: Chronic Allergies

• Treatment focuses on identifying and avoiding allergens, controlling symptoms with medications, and immunotherapy/hyposensitization. Teach patients that allergies are usually chronic with remissions and exacerbations and that therapy may reduce symptoms but does not completely eliminate sensitivity.

• Reduce exposure through environmental and lifestyle control, such as stress reduction, damp dusting, hypoallergenic mattress/pillow covers, air conditioning, masks outdoors, and avoiding known drug, pet, or airborne triggers. Patients with medication allergies should inform all health care providers and wear a Medic Alert bracelet.

• Patients at risk for anaphylaxis should carry epinephrine autoinjectors, preferably at least 2 doses, inject into the outer thigh at a 90° angle when symptoms occur, and call 911 after use for emergency evaluation and monitoring.

Latex Allergies

• Risk increases with frequent or prolonged latex exposure and can affect both patients and healthcare workers. Latex may be found in more than gloves, including BP cuffs, stethoscopes, tourniquets, IV tubing, syringes, electrode pads, oxygen masks, tracheal tubes, ostomy pouches, urinary catheters, anesthetic masks, and adhesive tape.

• Type IV reaction causes delayed allergic contact dermatitis, usually within 6–48 hours, with dryness, itching, fissuring, and cracked skin. Type I reaction occurs within minutes and may cause redness, hives, rhinitis, conjunctivitis, asthma, or anaphylactic shock.

• Latex-food syndrome occurs because some foods contain proteins similar to natural rubber latex. Foods associated with reactions include banana, avocado, chestnut, kiwi, tomato, water chestnut, guava, hazelnut, potato, peach, grapes, and apricot.

Human Immunodeficiency Virus Infection: Pathophysiology

• HIV is an RNA retrovirus that mainly attacks CD4+ T cells. It attaches to CD4, CCR5, and CXCR4 receptors, enters the cell, and uses reverse transcriptase to make DNA from its RNA.

• Integrase inserts the viral DNA into the CD4 cell’s DNA, causing the cell to make more HIV. Protease helps cut and assemble the new virus particles, which then leave the cell and eventually destroy it.

• As the CD4 count drops, the immune system becomes weaker. Counts above 500 cells/µL are generally healthier, problems increase below 500, and severe immunosuppression occurs below 200, greatly increasing the risk for opportunistic infections and cancers.

HIV Transmission: General

• Spread occurs through infected blood, semen, vaginal secretions, and breast milk. It is not spread through tears, saliva, urine, vomit, sputum, feces, sweat, respiratory droplets, hugging, dry kissing, shaking hands, sharing utensils, or toilet seats.

HIV Transmission: Sexual Transmission

• Unprotected sexual contact is the most common route, especially when the person with HIV has a high viral load. Tissue trauma and genital lesions from STIs such as herpes or syphilis increase transmission risk.

• A person with a sustained undetectable viral load does not sexually transmit HIV, known as U=U: Undetectable = Untransmittable.

HIV Transmission: Blood and Blood Products

• Spread can occur through sharing contaminated needles, syringes, straws, or other drug equipment. Transmission through donated blood is now very unlikely where routine HIV screening is performed.

• A needlestick involving HIV-infected blood carries about a 0.3% risk. Risk increases with a deep puncture, hollow-bore needle, visible blood, high viral load, or a device used for venous/arterial access; blood contacting intact skin is not a transmission route, while contact with broken skin carries some risk.

HIV Transmission: Perinatal Transmission

• A mother can transmit the virus to her baby during pregnancy, delivery, or breastfeeding. Without treatment, about 25% of infants born to mothers with HIV acquire it, but treatment with antiretroviral therapy (ART) can reduce the risk to less than 1%.

HIV Clinical Manifestations: Acute Infection

• Usually occurs about 2–4 weeks after infection and often looks like the flu or mono, with fever, swollen lymph nodes, sore throat, headache, fatigue, nausea, muscle/joint pain, diarrhea, and rash.

• The viral load is very high, so the person is most infectious during this stage. The CD4 count drops temporarily and then usually returns close to baseline.

HIV Clinical Manifestations: Chronic Infection

• During the asymptomatic phase, the person may have no symptoms or only mild signs for several years, but HIV is still active and can still be transmitted. Without treatment, the average time from initial infection to AIDS is about 10 years.

• During the symptomatic phase, the CD4 count falls closer to 200 cells/µL and viral load rises. Common symptoms include persistent fever, night sweats, chronic diarrhea, recurrent headaches, and severe fatigue.

• Signs that the disease is progressing include thrush, shingles, recurrent vaginal candidiasis, oral or genital herpes, bacterial infections, Kaposi sarcoma, and oral hairy leukoplakia.

AIDS

• The most advanced stage of HIV infection and is diagnosed when a person with HIV has a CD4 count below 200 cells/µL or develops a qualifying opportunistic infection, cancer, or wasting syndrome.

• Major opportunistic infections include Pneumocystis jirovecii pneumonia (PCP), TB, Mycobacterium avium complex (MAC), CMV disease, cryptococcosis, toxoplasmosis of the brain, severe candidiasis, and progressive multifocal leukoencephalopathy (PML). These infections become dangerous because the immune system is too weak to control organisms that normally would not cause severe disease.

• AIDS can also cause Kaposi sarcoma, invasive cervical cancer, certain lymphomas, wasting syndrome, and HIV-related cognitive or neurologic changes. Wasting syndrome means loss of at least 10% of ideal body mass, and multiple opportunistic diseases may occur at the same time.

HIV: Diagnostic Studies

• Diagnosis is made with HIV antibody/antigen testing using blood or saliva. The window period is about 3 weeks, when infection may be present but the test can still be negative; if recent risky exposure occurred despite a negative test, repeat testing in 4–6 weeks may be needed. A positive rapid test must be confirmed with a standard HIV assay.

• Disease progression is monitored using the CD4 count and viral load. Normal CD4 is about 800–1200 cells/µL and usually falls as HIV progresses; a lower viral load means less active disease. The goal of ART is an undetectable viral load, which means HIV is below the test’s detection level, not that the patient is cured.

• Common abnormal labs include low WBCs, lymphopenia, neutropenia, thrombocytopenia, anemia, and abnormal liver function tests. Patients should also be evaluated for hepatitis B and C coinfection, and genotype/phenotype resistance testing can help determine which ART drugs are most effective.

HIV Interprofessional Care

• Care focuses on monitoring disease progression and immune function, starting and monitoring ART, preventing and treating opportunistic infections, managing symptoms, reducing treatment complications, and preventing further HIV transmission.

• Ongoing assessment, patient teaching, support, and regular follow-up with the health care team are essential because HIV is a chronic infection that is controlled with treatment rather than cured.

Drug Therapy for HIV Infection: ART

• Antiretroviral therapy (ART) uses a combination of HIV medications to lower the viral load, maintain or increase CD4 cells, prevent opportunistic infections and symptoms, slow disease progression, and prevent transmission. When taken correctly and consistently, ART can reduce the viral load by about 90%–99%.

• Combination therapy uses drugs from different classes that block HIV at different parts of its replication cycle. This makes it harder for HIV to reproduce and develop drug resistance; resistance can develop quickly if medications are taken alone, skipped, or taken in inadequate doses.

• Major drug classes include attachment/entry inhibitors, integrase inhibitors, protease inhibitors, and reverse transcriptase inhibitors (NRTIs, NNRTIs, and NtRTIs). ART can have many drug interactions, including with antacids, proton pump inhibitors, OTC medications, herbal products, and supplements, so a complete medication history is important.

Drug Therapy for Opportunistic Diseases

• Prevention is the main goal because opportunistic diseases become more likely as the immune system weakens. ART, vaccines such as hepatitis A, hepatitis B, influenza, and pneumococcal vaccines, and disease-specific prevention measures can delay or prevent many infections.

• Once an opportunistic disease occurs, it may be difficult to completely eliminate, but prophylactic therapy can reduce illness and death. Better prevention and treatment of opportunistic diseases has greatly improved life expectancy in people with HIV.

Nursing Management - HIV Infection: Assessment

• For patients without known HIV, focus on risk factors for HIV, STIs, and blood-borne infections, including past blood transfusions before 1985, shared drug equipment, sexual exposure, previous STIs, and sexual contact with a person known to have HIV. Any positive answer should be explored further.

• For patients with HIV, the first visit should establish baseline data with a complete history and physical exam, immunization history, psychosocial assessment, and nutrition/diet evaluation.

• Repeat assessments regularly because risk factors, health status, and life circumstances can change over time.

Nursing Management - HIV Infection: Clinical Problems

• Major problems include risk for infection, deficient knowledge, difficulty coping, and poor nutritional status.

Nursing Management - HIV Infection: Planning

• Goals include helping the patient take ART correctly, maintain a healthy lifestyle, avoid other STIs and blood-borne infections, and prevent transmitting HIV to others.

• Support the patient in maintaining relationships, daily activities, productivity, and coping with HIV symptoms and treatment effects.

• Help the patient address spiritual concerns and feelings related to chronic illness, disability, and death.

Nursing Management - HIV Infection: Health Promotion

• Prevention focuses on helping patients develop safer, healthier, lower-risk behaviors. Prevention methods work best when they are used consistently and correctly.

• Teaching should be based on the patient’s individual risk behaviors and should be culturally sensitive, age-appropriate, and easy to understand, including discussion of sexual practices and drug use when relevant.

Nursing Management - HIV Infection: Biomedical Prevention

• PrEP (preexposure prophylaxis) is taken by people without HIV before exposure to reduce the risk of getting HIV through sex or IV drug use. It should be used with condoms, risk-reduction counseling, and regular HIV testing; options include Truvada or Descovy, taken daily.

• nPEP (nonoccupational postexposure prophylaxis) is started within 72 hours after a possible HIV exposure from sex, needlestick, or blood exposure. It usually involves combination ART for 28 days, followed by repeat HIV testing.

Nursing Management - HIV Infection: Behavior Modification

• Reduce sexual transmission by using condoms or dental dams, limiting sexual partners, and using PrEP when appropriate. Activities that avoid contact with blood, semen, and vaginal secretions have the lowest risk.

• Reduce drug-related transmission by not sharing needles, syringes, cookers, cotton, rinse water, straws, or pipes. Sterile equipment and needle-exchange programs help prevent HIV and other blood-borne infections.

• Pregnant patients with HIV should receive ART, which can lower perinatal transmission from about 25% to less than 1%. Health care workers should follow standard precautions, report blood exposures immediately, and receive PEP when indicated; routine voluntary HIV testing helps identify infection early.

Nursing Management - HIV Infection: Acute Care

• Early care focuses on starting and sticking with ART, watching for disease progression or opportunistic infections, preventing transmission, and teaching healthy habits. Missing even a few ART doses can lead to drug resistance, so adherence is extremely important.

• Teach patients to report new symptoms and medication side effects, use good hand hygiene, avoid new infections, maintain good nutrition, rest, exercise safely, avoid or limit alcohol/tobacco/drugs, and stay up to date on recommended vaccines. Newly diagnosed patients may need information repeated over time because fear, anxiety, depression, denial, anger, or guilt can affect learning.

• During acute exacerbations, continue ART and prophylactic therapy when ordered and treat the specific complication. For example, with PCP, focus on maintaining oxygenation; with cryptococcal meningitis, maintain safety if the patient is confused.

Nursing Management - HIV Infection: Ambulatory Care

• Care focuses on the patient’s physical, emotional, social, economic, and spiritual well-being. Assess for depression, grief, isolation, poor coping, and suicidal thoughts, and encourage counseling, support groups, and community resources when needed.

• HIV-related stigma and discrimination can cause loss of support, social isolation, low self-esteem, and financial problems. The Americans with Disabilities Act (ADA) protects people with HIV from discrimination in areas such as employment and housing.

• Manage symptoms and treatment side effects such as diarrhea, peripheral neuropathy, pain, nausea, vomiting, and fatigue. For diarrhea, focus on diet, fluids/electrolytes, and skin care; for fatigue, encourage energy conservation, planned rest, regular exercise, and avoiding caffeine, nicotine, and alcohol.

Gerontologic Considerations: HIV Infection

• Older adults with HIV may develop age-related conditions such as heart disease, cancer, diabetes, bone disease, hypertension, kidney disease, and cognitive problems at an earlier age. Management focuses on early detection, reducing modifiable risks, and adjusting ART when needed.

• Polypharmacy is a major concern because medications for chronic diseases may interact with ART. Nurses should closely monitor for drug interactions and adverse effects and recognize that stigma may prevent older adults from seeking care or support.

• During end-of-life care, nursing priorities are comfort, safety, emotional and spiritual support, and helping family/significant others cope with grief and loss.

Nursing Management - HIV Infection: Evaluation

• For patients at risk for HIV, expected outcomes are to develop and follow a plan to reduce personal risk factors and obtain HIV testing.

• For patients with HIV, expected outcomes are to adhere to treatment, work with the health care team to maintain the best possible health, and prevent transmission of HIV to others.

Rheumatoid Arthritis

• A chronic, systemic autoimmune disease causes inflammation of the synovial joints and usually follows periods of remission and exacerbation. It can also cause extraarticular problems outside the joints and may lead to major disability, loss of mobility, and decreased independence if not adequately treated.

• It occurs most often in women ages 30–60 and affects women about 3 times more often than men.

Rheumatoid Arthritis: Etiology and Pathophysiology

• The exact cause is unknown but likely involves genetics plus environmental triggers. An abnormal immune response produces rheumatoid factor (RF), an autoantibody that binds abnormal IgG, forming immune complexes that collect in the synovial joints and trigger inflammation.

• Complement, neutrophils, T helper (CD4) cells, macrophages, and inflammatory cytokines such as IL-1, IL-6, and TNF contribute to ongoing inflammation, thickening of the synovial lining, cartilage damage, and eventual joint destruction.

• HLA-DR4 and HLA-DR1 are strongly associated with genetic risk. Smoking increases the risk of developing RA and decreases the chance of remission, while smoking cessation lowers risk.

Rheumatoid Arthritis: Clinical Manifestations

• Joint involvement is usually bilateral and symmetric, commonly affecting the PIP, MCP, and MTP joints first. Expect pain, warmth, swelling, limited motion, and morning stiffness lasting at least 60 minutes and sometimes several hours; stiffness may improve with activity.

• As disease progresses, chronic inflammation can cause pannus formation, cartilage and bone destruction, subluxation, muscle atrophy, and joint deformities. Classic deformities include ulnar drift, swan-neck deformity, boutonnière deformity, and hallux valgus; wrist inflammation may also cause carpal tunnel symptoms and decreased grip strength.

• Extraarticular findings include firm, nontender rheumatoid nodules, increased cardiovascular risk, Sjögren syndrome with dry/gritty eyes, and Felty syndrome, which causes splenomegaly and low WBCs and increases the risk for infection.

Rheumatoid Arthritis: Diagnostic Studies

• Diagnosis is based on history, physical exam, joint involvement, symptom duration, and lab findings. A classification score of 6 or more out of 10 supports definite RA.

• Rheumatoid factor (RF) is positive in about 80% of patients, but a negative result does not rule out RA. Anti-CCP is more specific for RA, and positive RF plus anti-CCP strongly supports the diagnosis. ESR and CRP increase with active inflammation and help monitor disease activity; ANA may be elevated but is not specific.

• X-rays alone do not diagnose RA. Early findings may show soft-tissue swelling and bone demineralization, while later disease can show joint-space narrowing, cartilage destruction, erosions, subluxation, deformity, poor alignment, and fusion. Baseline x-rays help track progression, while bone scans are better for detecting early joint changes.

Rheumatoid Arthritis: Stages

• Stage I: Inflammation is present in the tissues around the joints and may cause joint pain or stiffness, although destructive changes may not yet be visible on x-ray. Osteoporosis may be present, but there is no cartilage or bone destruction.

• Stage II: Ongoing inflammation begins to cause cartilage and slight bone destruction, leading to increased stiffness, decreased range of motion, muscle atrophy, and possible nodules or tenosynovitis. There is still no joint deformity.

• Stage III: Inflammation has caused significant cartilage and bone destruction, with more pain, stiffness, decreased ROM, joint deformity, osteoporosis, and extensive muscle atrophy. Physical joint changes are usually visible, but there is no joint fusion.

• Stage IV: Inflammation may decrease or stop, but structural joint damage continues to worsen. Severe pain, swelling, stiffness, and loss of mobility may occur, with all Stage III findings plus fibrous or bony joint fusion.

Rheumatoid Arthritis: Drug Therapy

• DMARDs slow RA progression and help prevent joint damage and deformity. Methotrexate is the preferred early treatment and usually begins working in 4–6 weeks; monitor CBC, liver, and kidney function, and avoid pregnancy. Other DMARDs include hydroxychloroquine, sulfasalazine, and leflunomide.

• Biologic response modifiers are often used for moderate to severe RA when DMARDs are not enough. They suppress parts of the immune/inflammatory response, so screen for TB before treatment, monitor closely for infection, and avoid live vaccines.

• Corticosteroids can temporarily control inflammation during flares or while waiting for DMARDs to work, but they do not stop disease progression and long-term use can cause osteoporosis. NSAIDs and aspirin relieve pain and inflammation but also do not slow RA progression; nonaspirin NSAIDs increase the risk for blood clots, heart attack, and stroke.

Rheumatoid Arthritis: Surgical Therapy

• Surgery may be needed when there is severe pain or major joint deformity with loss of function. Options include synovectomy, which removes the inflamed joint lining, and arthroplasty, or total joint replacement, to improve joint function and relieve pain.

Nursing Management - Rheumatoid Arthritis: Assessment

• Assess joint pain, swelling, range of motion, mobility, and overall health status, along with how RA affects daily function and independence.

• Also assess family support, emotional stress, sexual concerns, finances, work limitations, transportation, and needed home/work modifications.

• Use identified problems to develop a rehabilitation and education plan with the interprofessional team.

Nursing Management - Rheumatoid Arthritis: Clinical Problems

• Major problems include impaired musculoskeletal function, pain, and impaired role performance related to joint inflammation, stiffness, deformity, and decreased mobility.

Nursing Management - Rheumatoid Arthritis: Planning

• Goals are to achieve acceptable pain control, preserve as much joint function as possible, and maximize independence with self-care.

• The patient should participate in planning and following the treatment plan while maintaining a positive self-image.

Nursing Management - Rheumatoid Arthritis: Implementation

• Care includes medications, exercise, rest, joint protection, heat/cold therapy, relaxation, and patient teaching. Teach patients to balance activity with rest and use strategies that protect joints while maintaining as much independence as possible.

• Give NSAIDs, DMARDs, BRMs, and other medications as ordered, and teach their purpose, side effects, and required lab monitoring. DMARDs and BRMs increase infection risk, and carefully timing medications can help reduce early-morning stiffness and pain.

• Work with physical therapy for mobility, exercise, assistive devices, and thermal treatments; occupational therapy for self-care devices and home/work modifications; and social work for equipment, financial concerns, and vocational needs. Assist with ROM and self-care as needed.

Rheumatoid Arthritis - Implementation: Rest

• Pace activities by alternating activity with scheduled rest and rest before becoming exhausted. Avoid prolonged bed rest because it increases stiffness and immobility complications.

• Maintain good alignment with a firm mattress and encourage extension rather than flexion. Never place pillows under the knees because this increases the risk for flexion contractures.

Rheumatoid Arthritis - Implementation: Joint Protection

• Reduce joint stress by using the strongest joints available, distributing weight across several joints, avoiding repetitive movements and heavy lifting, changing positions often, and keeping joints in a neutral position.

• Use splints and assistive devices to protect joints and increase independence. Remove splints regularly to check the skin and perform ROM exercises, then reapply as prescribed.

Rheumatoid Arthritis - Implementation: Cold and Heat Therapy

• Use cold during periods of increased inflammation to decrease pain and swelling; apply for only 10–15 minutes at a time.

• Moist heat is better for chronic stiffness and can be applied for up to 20 minutes. Avoid combining an external heat source with heat-producing creams such as capsaicin because of burn risk.

Rheumatoid Arthritis - Implementation: Exercise

• Gentle daily ROM and therapeutic exercise help maintain joint movement, muscle strength, and endurance. Too little movement causes stiffness and weakness, while overaggressive exercise can increase pain, inflammation, and joint damage.

• During acute inflammation, limit exercise to about 1–2 repetitions. Warm-water exercise can make movement easier, but walking or swimming does not replace prescribed therapeutic exercise.

Rheumatoid Arthritis - Implementation: Nutrition

• Encourage a balanced diet and healthy weight because excess weight increases stress on affected joints. Pain, fatigue, depression, and limited mobility can cause weight loss, while corticosteroids can increase appetite and cause weight gain.

• Corticosteroids may cause Cushing-like changes such as moon face and fat redistribution. Teach patients not to abruptly stop or change the corticosteroid dose.

Rheumatoid Arthritis - Implementation: Psychologic Support

• Assess how chronic pain, disability, role changes, sexuality, finances, and loss of independence affect coping. Encourage counseling, support groups, family/community support, and vocational or home-care resources as needed.

• Chronic pain and loss of function can contribute to depression and make patients vulnerable to unproven treatments. Helpful strategies include exercise, music, reading, counseling, biofeedback, and hypnosis.

Arthritis: Gerontologic Considerations

• Older adults may have multiple types of arthritis, and age-related changes can make tests such as RF and ESR harder to interpret. Pain and weakness may also be related to depression or inactivity, not only joint disease.

• Older adults are more sensitive to medication effects. NSAIDs increase the risk for GI bleeding and kidney toxicity, while polypharmacy increases drug-interaction risk, so medication regimens should be kept as simple as possible.

• Corticosteroids can worsen age-related bone loss, increasing the risk for osteopenia and fractures, especially vertebral compression fractures. Age-appropriate exercise and a strong support system help maintain function and treatment adherence.

Systemic Lupus Erythematosus

• A chronic, multisystem autoimmune inflammatory disease caused by a combination of genetic, hormonal, environmental, and immune factors. It has an unpredictable course with periods of remission and exacerbation.

• It commonly affects the skin, joints, pleura, and pericardium, but can also involve the kidneys, blood, and nervous system.

• About 90% of patients are women, and it most often develops between ages 15–45 years.

Systemic Lupus Erythematosus: Etiology and Pathophysiology

• The exact cause is unknown, but genetics, hormones, infections, and environmental triggers contribute. HLA-DR2 and HLA-DR3 are associated with SLE, and symptoms may worsen with pregnancy/postpartum changes, UV light, stress, infections, and certain medications.

• The immune system makes autoantibodies, especially antinuclear antibodies (ANA) and antibodies against DNA. These antibodies form immune complexes that deposit in tissues and trigger inflammation.

• SLE is a Type III hypersensitivity reaction. Immune-complex inflammation can damage the kidneys, heart, skin, brain, joints, and other organs.

Clinical Manifestations of Lupus: Skin

• Common findings include photosensitivity, butterfly (malar) rash across the cheeks and nose, discoid lesions, oral or nasal ulcers, and alopecia. Skin lesions often worsen with sun or UV exposure.

Clinical Manifestations of Lupus: Musculoskeletal

• Patients commonly have polyarthralgia, morning stiffness, joint swelling, and nonerosive arthritis. Joint deformities such as swan-neck deformity, ulnar deviation, and subluxation can occur, and patients have an increased risk for bone loss and fractures.

Clinical Manifestations of Lupus: Cardiopulmonary

• Problems can include pleuritis, pleural effusion, pericarditis, myocarditis, endocarditis, dysrhythmias, cough, and tachypnea. Antiphospholipid syndrome can cause arterial and venous clots, increasing the risk for stroke, MI, and gangrene.

Clinical Manifestations of Lupus: Renal

• Kidney involvement may cause proteinuria, hematuria, and glomerulonephritis and can progress to permanent kidney damage or ESRD. About 40% of patients develop renal problems, often within the first 5 years after diagnosis.

Clinical Manifestations of Lupus: Neurologic

• Neurologic problems can include headaches, seizures, stroke, peripheral neuropathy, psychosis, confusion, anxiety, depression, and cognitive impairment. Clotting from antiphospholipid antibodies can contribute to stroke, while inflammation can cause more widespread neuropsychiatric symptoms.

Clinical Manifestations of Lupus: Hematologic and Infection

• Blood abnormalities can include anemia, leukopenia, lymphopenia, thrombocytopenia, and abnormal bleeding or clotting. Patients also have an increased risk for infection, especially when taking immunosuppressive drugs; live vaccines should be avoided with corticosteroid or cytotoxic therapy.

Systemic Lupus Erythematosus: Diagnostic Studies

• There is no single diagnostic test for SLE; diagnosis is based on clinical findings and laboratory results. ANA is positive in about 97% of patients, making it very sensitive but not specific. More specific tests include anti-dsDNA, which is associated with lupus nephritis, and anti-Smith (Sm) antibodies, which are highly specific for SLE. Antiphospholipid antibodies may also be present.

• ESR may be elevated with lupus or other inflammatory conditions, while C3 and C4 complement levels may be low during active disease. Serial anti-dsDNA titers and complement levels can help monitor disease activity; ESR and CRP may also help assess inflammation and treatment response.

• Urinalysis may show proteinuria or hematuria when the kidneys are involved, and fluid assessment may reveal edema. A chest X-ray may show fluid or inflammation in the lungs. High-yield clue: SLE + proteinuria and hematuria = think lupus nephritis.

Systemic Lupus Erythematosus: Drug Therapy

• NSAIDs are used for mild joint pain but require monitoring for GI bleeding and kidney problems. Hydroxychloroquine helps with fatigue, skin problems, joint symptoms, and reducing flares; patients need an eye exam every 6–12 months because of the risk for retinopathy.

• Corticosteroids are used for flares or severe disease and should be given at the lowest dose for the shortest time possible. They must be tapered slowly and never stopped abruptly.

• Immunosuppressants such as azathioprine and cyclophosphamide help prevent organ damage but increase toxicity and infection risk. Anticoagulants may be used when clotting is a concern, while anti-DNA levels and complement levels can help monitor disease activity and treatment response.

Nursing Management - Lupus: Assessment

• Assess how pain and fatigue affect ADLs. During a flare, closely monitor fever, joint inflammation, ROM, pain, fatigue, weight, fluid intake, and urine output.

• Watch for renal problems and fluid retention, especially with corticosteroid use; collect 24-hour urine for protein and creatinine clearance as ordered. Also assess for bleeding such as pallor, bruising, petechiae, and black/tarry stools.

• Perform frequent neurologic assessments for vision changes, headaches, personality changes, seizures, memory loss, numbness, tingling, and weakness. Psychosis may be caused by CNS lupus or corticosteroid therapy.

Nursing Management - Lupus: Clinical Problems

• Major clinical problems include musculoskeletal problems, impaired role performance, and impaired tissue integrity related to inflammation, pain, fatigue, skin involvement, and other effects of SLE.

Nursing Management - Lupus: Planning

• Goals are to achieve acceptable pain control, avoid activities or triggers that worsen SLE, and maintain the best possible daily function.

• The patient should also work toward maintaining normal roles, independence, and a positive self-image despite the chronic disease.

Nursing Management - Lupus: Implementation

• Teach the patient and caregiver that SLE is unpredictable, so following the treatment plan does not completely prevent flares. Common flare triggers include fatigue, sun exposure, emotional stress, infection, certain drugs, and surgery.

• Encourage active self-management and trigger avoidance, and explain the disease, treatments, and diagnostic procedures in simple terms.

• Teach the purpose, correct use, and side effects of medications. Patients should not abruptly stop prescribed drugs, because this can worsen disease activity.

Nursing Management - Lupus: Role Performance

• Provide emotional support, especially during flares, because SLE can affect work, school, relationships, recreation, and future plans.

• Help the patient set realistic goals for mobility, energy, and self-esteem and plan activities around fatigue, sun restrictions, and physical limitations.

• Encourage open communication with employers, teachers, coworkers, and family about how SLE may affect daily responsibilities and needed accommodations.

Nursing Management - Lupus: Pregnancy

• Pregnancy should ideally be planned when SLE disease activity is minimal. Some drugs, such as methotrexate, must be stopped or changed before pregnancy, while hydroxychloroquine can usually be continued safely.

• Pregnancy carries increased risks for spontaneous abortion, stillbirth, and intrauterine growth restriction because immune complexes and inflammation can affect placental blood vessels.

• Pregnancy can worsen renal, lung, CNS, and cardiovascular involvement, and postpartum flares are common. Women with severe organ involvement may be advised against pregnancy.

Nursing Management - Lupus: Evaluation

• Expected outcomes include using energy-conservation techniques and adjusting daily activities to match the patient’s current energy level.

• The patient should maintain skin integrity with prescribed topical treatments and help prevent flares by using sunscreen and limiting sun exposure.

Antiphospholipid Syndrome (APS)

• Develops when antiphospholipid antibodies increase the tendency for abnormal blood clotting, raising the risk of both arterial and venous thrombosis.

• Can cause DVT, PE, stroke, other arterial/venous clots, and pregnancy complications.

• High-yield clue: Lupus + unexplained clotting or pregnancy complications = think APS.

Raynaud Phenomenon

• Causes the fingers and/or toes to change color with cold exposure or stress because of abnormal vasoconstriction that temporarily reduces blood flow.

• Promote circulation by keeping the extremities warm, avoiding cold exposure, and managing stress.

• Avoid smoking, because nicotine causes vasoconstriction and can worsen symptoms.

SLE Diagnosis

• Diagnosis is supported when 4 or more criteria are present, including abnormal ANA, discoid rash, malar/butterfly rash, oral ulcers, photosensitivity, nonerosive arthritis involving 2 or more joints, pleuritis/pericarditis, neurologic disorders such as seizures or psychosis, and renal involvement such as persistent proteinuria or cellular casts.

• Hematologic findings can include hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia. Immunologic findings can include anti-DNA antibodies, antibodies to nuclear antigens, or positive antiphospholipid antibodies.

• Serial anti-DNA titers and serum complement levels can help monitor disease activity and management; ESR and CRP may also be helpful.

HIV Medication: Abacavir

• Can cause a severe hypersensitivity reaction in patients with the HLA-B*5701 allele, so testing is done before starting.

• Symptoms include fever, rash, GI symptoms, respiratory symptoms, and malaise.

• If a true hypersensitivity reaction occurs, NEVER restart the medication.

HIV Medications: NRTIs

• Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) interfere with HIV DNA formation by acting as faulty building blocks that stop the developing viral DNA chain.

• They act during reverse transcription, when HIV is converting its RNA into DNA. Examples from your PowerPoint include tenofovir, emtricitabine, and abacavir.

• High-yield: NRTIs stop DNA-chain formation.

HIV Medications: NNRTIs

• Non-nucleoside reverse transcriptase inhibitors (NNRTIs) bind to and inhibit the reverse transcriptase enzyme, preventing HIV RNA from being converted into DNA.

• Examples from your PowerPoint include efavirenz, rilpivirine, and doravirine.

• High-yield distinction: NRTIs interfere with the DNA chain; NNRTIs directly inhibit the reverse transcriptase enzyme.

HIV Medications: Attachment & Entry Inhibitors

• Attachment inhibitors interfere with HIV attaching to the CD4 cell, while other entry inhibitors prevent the virus from successfully entering the cell.

• These medications act at one of the earliest stages of the HIV life cycle, before viral replication can occur inside the host cell.

• High-yield: Attachment/entry inhibitors keep HIV outside the CD4 cell. Fall 2026 - Immunity – HIV NIH describes attachment inhibitors as interfering with the interaction between viral gp120 and the CD4 receptor.

HIV Medications: Integrase Inhibitors

• Integrase inhibitors block the integrase enzyme, preventing newly formed viral DNA from being inserted into the DNA of the host CD4 cell.

• Without integration into the host genome, HIV cannot effectively use the cell to produce more virus.

• High-yield: Integrase inhibitors prevent viral DNA from joining host DNA.

HIV Medications: Protease Inhibitors

• Protease inhibitors block the protease enzyme that normally cuts long viral proteins into the smaller functional proteins needed to make a mature infectious virus.

• Examples from your PowerPoint include darunavir and atazanavir.

• High-yield: Protease inhibitors prevent viral maturation, so newly produced virus particles are not properly functional.

HIV Opportunistic Infection: Pneumocystis jirovecii Pneumonia (PJP/PCP)

• Classically associated with CD4 counts below 200 cells/mm³ and causes fever, progressive dyspnea, dry/nonproductive cough, and hypoxemia.

• The patient may have significant respiratory distress even though the cough is not producing much sputum.

HIV Opportunistic Infection: Toxoplasmosis

• Usually occurs with advanced immunosuppression and commonly affects the brain.

• Can cause headache, altered mental status, seizures, focal neurologic deficits, and brain lesions.

HIV Opportunistic Infection: CMV Retinitis

• Advanced immunosuppression can allow CMV to infect the retina and threaten vision.

• Watch for floaters, blurred vision, visual-field changes, or vision loss.

HIV Opportunistic Infection: Cryptococcal Meningitis

• Occurs primarily with advanced immunosuppression and involves the CNS.

• Causes headache, fever, neck stiffness, photophobia, and altered mental status.

HIV Opportunistic Infection: Mycobacterium avium Complex (MAC)

• Usually occurs with advanced immunosuppression, especially when the CD4 count is below 50 cells/mm³.

• Common findings include fever, night sweats, weight loss, fatigue, diarrhea, and abdominal symptoms; disseminated disease can involve multiple organs.

HIV Opportunistic Infection: Tuberculosis (TB)

• People with HIV have an increased risk of developing active TB, and disease may be pulmonary or extrapulmonary, especially with greater immunosuppression.

• Common symptoms include persistent cough, fever, night sweats, weight loss, and hemoptysis.

HIV Opportunistic Infection: Candidiasis

• Oral thrush causes creamy or white plaques in the mouth and is most commonly seen when the CD4 count is below 200 cells/mm³.

• Esophageal candidiasis causes painful swallowing, difficulty swallowing, or retrosternal pain and represents more advanced immune suppression.

HIV-Associated Kaposi Sarcoma

• An AIDS-defining cancer associated with HHV-8 that commonly causes red, purple, or brown vascular lesions on the skin or oral mucosa.

• Disease may also involve internal organs such as the lungs or GI tract, causing symptoms such as dyspnea or GI bleeding.