NLE Immune System & Immunologic Disorders — Autoimmune Disorders and HIV/AIDSSummary

Immunity is the body's ability to resist and defend against foreign substances (antigens). Innate immunity is present from birth, responds the same way to any invader (nonspecific), and provides immediate protection through physical barriers (skin, mucous membranes), phagocytic cells (neutrophils, macrophages), inflammation, and the complement system. It has no memory. Adaptive immunity develops over time, is antigen-specific, creates immunologic memory, and therefore responds faster and stronger on re-exposure. It comprises two arms: humoral immunity (B lymphocytes producing antibodies) and cell-mediated immunity (T lymphocytes: CD4 helper cells and CD8 cytotoxic cells). In clinical practice, understanding this distinction helps explain why vaccinated patients show rapid protective responses while first-time infections require time for adaptive immunity to mount.

B lymphocytes (plasma cells) produce five classes of antibody, each with distinct roles: IgG is the most abundant immunoglobulin, crosses the placenta to provide passive immunity to newborns, and mediates the secondary (memory) response to antigen re-exposure—this is why booster vaccines work. IgM is the largest antibody and is always the first produced in an acute (primary) infection; it does not cross the placenta, so its presence in a newborn indicates in-utero infection. IgA is the main antibody in secretions (saliva, tears, breast milk, mucous membranes, respiratory and gastrointestinal secretions) and protects mucosal surfaces; this is why breastfeeding provides specific protection against enteric and respiratory pathogens. IgE mediates allergic and anaphylactic (type I) reactions by binding to mast cells and basophils; on re-exposure to allergen, crosslinking of IgE triggers massive mediator release. IgD serves as a surface receptor on B cells and has the least understood role. In Philippine healthcare, understanding IgA deficiency is important because such patients cannot mount mucosal immunity and are prone to recurrent respiratory and gastrointestinal infections.

Acquired immunity is further classified into four categories based on how and when antibodies are obtained. Natural active immunity results when the body makes its own antibodies after actual exposure to antigen (e.g., illness with chickenpox or measles); onset is slow (days to weeks) but the response is long-lasting (years to lifetime) because immunologic memory is formed. Artificial active immunity results when the body makes its own antibodies after a vaccine containing attenuated or killed antigen (e.g., MMR, tetanus toxoid, COVID-19 vaccine); onset is slow but duration is long-lasting, hence booster schedules. Natural passive immunity occurs when ready-made maternal antibodies (IgG) cross the placenta during pregnancy or IgA passes through breast milk; onset is immediate but duration is temporary (weeks to months) as these antibodies degrade. Artificial passive immunity is given by injection of ready-made immunoglobulin (e.g., tetanus immunoglobulin, hepatitis B immunoglobulin, antivenom, rabies immunoglobulin); onset is immediate but short-lived (weeks) because the body produces no memory. The core clinical rule: active immunity is slow but durable (develops memory); passive immunity is fast but fleeting (no memory formed). This distinction is crucial for understanding vaccination schedules, post-exposure prophylaxis protocols, and newborn protection strategies used across Philippine healthcare facilities.

Hypersensitivity is an exaggerated or inappropriate immune response to an antigen that causes tissue damage. The Gell and Coombs classification organizes them into four types using the memory aid ACID: Type I is Anaphylactic/Allergic, mediated by IgE; Type II is Cytotoxic, mediated by IgG or IgM antibodies directed against cell-surface antigens; Type III is Immune Complex deposition; Type IV is Delayed cell-mediated (T-cell) reaction. Type I, II, and III are antibody-mediated and generally occur within minutes to hours (rapid); Type IV is T-cell-mediated and occurs over 24–72 hours (delayed). Type I reactions involve sensitization on first exposure, then on re-exposure the allergen binds to IgE on mast cells and basophils, triggering degranulation and release of histamine and other mediators—this causes immediate vasodilation, increased capillary permeability, bronchoconstriction, and smooth muscle contraction. Type II reactions destroy the person's own cells through complement-mediated lysis or phagocytosis (e.g., ABO blood transfusion reactions, hemolytic disease of the newborn). Type III involves immune complex deposition in tissues and vessels, activating complement and causing inflammation (e.g., systemic lupus erythematosus, post-streptococcal glomerulonephritis). Type IV is the only non-antibody-mediated hypersensitivity; sensitized T lymphocytes recognize antigen, release cytokines, recruit macrophages, and produce delayed inflammation (e.g., PPD/tuberculin skin test, contact dermatitis from poison ivy or latex, transplant rejection). This classification is fundamental to Philippine nursing practice because different hypersensitivities require different management strategies—anaphylaxis requires immediate epinephrine, while contact dermatitis requires only supportive care.

Allergy is a Type I hypersensitivity to an ordinarily harmless environmental antigen (allergen). Common allergens in the Philippines include pollen, dust mites, mold spores (especially prevalent during rainy season), animal dander (dogs, cats), foods (peanuts, shellfish, eggs, cow's milk), insect venom (bee, wasp, mosquito), medications (penicillin is the classic drug allergy), and latex. Manifestations vary by route of exposure: respiratory allergens cause sneezing, rhinorrhea (runny nose), nasal congestion, wheezing, dyspnea, and cough; ingested allergens cause nausea, vomiting, cramping, diarrhea, and oral pruritus; injected allergens (drugs, venom) may cause systemic reactions including anaphylaxis; skin contact causes urticaria (hives), pruritus, erythema, and angioedema (swelling of lips, tongue, face, eyelids—dangerous if airway involved). Diagnosis relies on detailed allergy history (specific allergen, timing of reactions, prior severity), skin testing (scratch, prick, or intradermal—a wheal-and-flare indicates IgE sensitization), serum-specific IgE (RAST), and complete blood count (eosinophilia supports allergic process). Pharmacotherapy includes antihistamines (first-generation such as diphenhydramine cause drowsiness; second-generation such as cetirizine or fexofenadine are less sedating), corticosteroids (intranasal or systemic for moderate-to-severe allergy), mast cell stabilizers (cromolyn), and leukotriene modifiers (montelukast) for prophylaxis. Patient education includes allergen avoidance, reading labels, informing healthcare providers, and for severe allergies, carrying an epinephrine auto-injector. This knowledge is essential for nurses in Philippine community health centers, clinics, and hospitals, where allergy management is a first-line intervention.

Anaphylaxis is a severe, rapid, systemic Type I hypersensitivity reaction that is life-threatening and requires immediate intervention. It is triggered by massive IgE-mediated degranulation of mast cells and basophils, releasing histamine, tryptase, leukotrienes, and prostaglandins. These mediators cause widespread vasodilation and increased vascular permeability (leading to distributive shock and profound hypotension), bronchoconstriction with severe bronchospasm, laryngeal edema, increased mucus production, and smooth muscle contraction. Onset is within seconds to minutes of allergen exposure. Early signs include a sense of impending doom, pruritus, flushing, urticaria (hives), and angioedema. Progression includes throat tightness, hoarseness, stridor, and laryngeal edema (leading cause of anaphylaxis death—airway obstruction must be prevented or treated immediately), wheezing and dyspnea from bronchoconstriction, tachycardia and severe hypotension from shock, dizziness, syncope, and cardiovascular collapse. The single most important drug is epinephrine. Adult dose: 0.3–0.5 mg of 1:1000 (1 mg/mL) solution intramuscularly (not intravenously), administered into the anterolateral thigh (vastus lateralis muscle); repeat every 5–15 minutes as needed. Pediatric dose: 0.01 mg/kg IM up to 0.3 mg. Epinephrine causes alpha-adrenergic vasoconstriction (raises blood pressure and reverses shock), beta-adrenergic bronchodilation (opens airways), and reversal of laryngeal edema. A critical NLE teaching point: use 1:1000 concentration IM for anaphylaxis; use 1:10,000 IV only for cardiac arrest—confusing these concentrations is a common error. Supportive care includes maintaining a patent airway (high-flow oxygen, prepare for intubation/emergency cricothyrotomy), removing or stopping the trigger (stop IV, remove stinger), positioning supine with legs elevated (unless breathing compromised), establishing IV access and giving rapid crystalloid fluids. Adjunct medications (antihistamines, H2 blockers, corticosteroids, bronchodilators) are secondary and none replaces epinephrine. Monitor continuously for a biphasic (late-phase) reaction that can recur hours after apparent recovery. Patient teaching includes carrying an epinephrine auto-injector, self-administration technique, seeking emergency care after every use, wearing a medical-alert bracelet, and strict allergen avoidance. This is the most heavily tested emergency topic in the NLE; every Filipino nurse must be able to recognize and treat anaphylaxis within seconds.

Latex allergy is increasingly important in the Philippines due to widespread use of latex gloves and equipment in healthcare. Latex can trigger two distinct immune responses: Type IV delayed contact dermatitis (most common) and Type I immediate IgE-mediated reaction (most dangerous). The Type IV reaction manifests as an eczematous, itchy rash 24–48 hours after latex contact; it is uncomfortable but not life-threatening. The Type I reaction can occur within minutes of exposure and progress from urticaria and rhinitis to asthma, angioedema, and anaphylaxis—this form can be fatal. At-risk groups include healthcare workers (repeated glove exposure), patients with spina bifida (multiple catheterizations and surgeries from infancy), patients with a history of multiple surgical procedures, and patients with occupational glove exposure. A well-documented latex-food cross-reactivity exists: patients allergic to latex often react to banana, avocado, kiwi, and chestnut because these fruits share similar allergenic proteins. Nursing implications for hospitalized latex-sensitive patients include: identifying the allergy on admission and using a latex-free environment (non-latex gloves, equipment, catheters, dressings, and supplies); scheduling latex-sensitive patients as the first case of the day to minimize airborne latex particles from prior surgeries; keeping emergency anaphylaxis supplies (epinephrine, oxygen, airway equipment) immediately available; and avoiding cross-contamination from healthcare workers who have handled latex immediately before touching the patient. Patient education includes recognizing latex in gloves, medical equipment, some condoms, and even some foods; informing all healthcare providers; and understanding the risk of anaphylaxis. This knowledge is essential for safe, inclusive practice in Philippine hospitals and clinics where latex-free environments are becoming a standard of care.

Immunodeficiency is a deficient immune response that leaves the person vulnerable to infection, opportunistic pathogens, and malignancy. It is classified as primary (congenital, inherited) or secondary (acquired). Primary immunodeficiency is present from birth due to genetic defects: severe combined immunodeficiency (SCID) affects both B and T cells (the historic 'bubble boy' disorder), selective IgA deficiency leaves mucosal surfaces unprotected, Bruton agammaglobulinemia affects B-cell development, and DiGeorge syndrome (22q11 deletion) affects T-cell and thymic development. Primary deficiencies are rare but are high-yield NLE topics. Secondary immunodeficiency is far more common and results from other conditions or treatments: HIV/AIDS is the classic example and the most common cause of significant immunodeficiency worldwide (affects CD4 helper cells, leading to opportunistic infections if CD4 count falls below 200); malignancy (leukemia, lymphoma) damages immune cells; chemotherapy and radiation therapy suppress immune cell production; immunosuppressive drugs (corticosteroids, transplant rejection prophylaxis) dampen immune responses; malnutrition impairs immune function; splenectomy removes a major lymphoid organ; and advanced age causes immune senescence. Nursing management includes protective/neutropenic precautions: meticulous hand hygiene by all staff, private room (if severely immunocompromised), avoiding crowds and people with active infections, and for severely neutropenic patients, avoiding raw fruits/vegetables, fresh flowers, and standing water (sources of environmental organisms). Monitor closely for subtle signs of infection—fever may be the only sign of serious infection in immunocompromised patients; report promptly; cultures should be obtained before antibiotic initiation. Ensure vaccinations are current where appropriate; live vaccines (MMR, varicella, yellow fever) are generally contraindicated in significant immunodeficiency because the vaccine virus can cause disease. Immunoglobulin replacement (IVIG) may be given for antibody deficiencies; infuse slowly and monitor for infusion reactions. Teach infection prevention, optimal nutrition, rest, stress management, and the importance of reporting early symptoms. In Philippine healthcare, secondary immunodeficiency from untreated HIV and malnutrition remains a significant burden; nurses must recognize at-risk populations and implement protective measures.

Using the nursing process (assessment, diagnosis, planning, implementation, evaluation) aligned with NANDA International nursing diagnoses and NCM (Nursing Care Management) levels, nurses systematically address immunologic disorders. For allergic patients, relevant NANDA diagnoses include: Risk for Allergy Response (related to known allergen exposure), Ineffective Health Maintenance (related to lack of knowledge about allergen avoidance), and Anxiety (related to fear of anaphylaxis). For anaphylaxis, diagnoses include Ineffective Airway Clearance (related to laryngeal edema), Decreased Cardiac Output (related to distributive shock), and Risk for Decreased Tissue Perfusion. For immunodeficiency, diagnoses include Risk for Infection (related to impaired immune function), Ineffective Health Maintenance (related to need for protective precautions), and Deficient Knowledge (related to disease management). NCM levels guide intervention intensity: Level 1 (basic assessment and monitoring, suitable for community or primary care settings), Level 2 (skilled nursing care with moderate complexity, typical for clinic or ward settings), and Level 3 (complex, highly specialized care, typical for ICU or tertiary care). Assessment always includes a detailed allergy history (specific allergen, timing, prior reaction severity, medications), family history of atopy, and current immunization status. Planning prioritizes using Maslow's hierarchy: physiologic safety (airway patency, breathing, circulation) is top priority in anaphylaxis; then safety needs (avoiding allergens, preventing infection in immunocompromised); then love and belonging needs (family support, social connection); then esteem needs (confidence in self-management); then self-actualization (full participation in life activities). Implementation varies by disorder but always includes patient education, medication administration per protocol (particularly epinephrine in anaphylaxis), monitoring, and documentation per RA 9173 standards. Evaluation assesses whether nursing interventions achieved desired outcomes (e.g., absence of allergic reaction, patient correctly demonstrates epinephrine auto-injector use, no signs of infection in immunocompromised patient). This systematic approach ensures comprehensive, evidence-based care aligned with Philippine nursing standards.

Innate immunity (physical barriers, phagocytes, complement, inflammation) acts as the first line of defense and initially contains an infection. This gives the adaptive immune system time to develop antigen-specific responses. If innate immunity fails (e.g., skin break, neutropenia), the person becomes highly susceptible to infection before adaptive immunity can mount a response. Understanding this relationship explains why healthcare-acquired infections are common when patients have impaired skin integrity, wounds, or low neutrophil counts.

On first allergen exposure, B cells produce IgE specific to that allergen; IgE binds to mast cells and basophils. On re-exposure, allergen crosslinks IgE, triggering massive degranulation and mediator release. If the reaction is localized (urticaria, rhinitis, asthma), it is a simple allergy. If the reaction is systemic and severe (hypotension, airway edema, shock), it is anaphylaxis—a medical emergency requiring immediate epinephrine. This progression explains why the first allergic reaction may be mild but subsequent exposures can be more severe, and why anaphylaxis can develop within minutes.

Latex exposure can trigger either a Type IV delayed T-cell response (causing eczematous dermatitis 24–48 hours later) or a Type I immediate IgE response (causing urticaria, asthma, anaphylaxis within minutes). The same patient may experience both reactions at different times or on different exposures. Understanding this explains why some latex-allergic people get a rash (Type IV) while others have life-threatening reactions (Type I), and why type I reactions are more dangerous and require emergency preparedness in clinical settings.

Active vaccination (artificial active immunity) introduces antigen that stimulates B cell proliferation and memory formation. On first vaccine dose, antibodies (usually IgM then IgG) are produced slowly over weeks; protection is incomplete. On booster doses, memory B cells rapidly produce high-affinity IgG (secondary response) within days. This explains why booster schedules are timed as they are and why vaccination protects longer than a single dose. Understanding this relationship is critical for teaching patients why vaccination schedules matter and why some people need boosters after injury (tetanus prophylaxis) or exposure.

In primary immunodeficiency (e.g., SCID, IgA deficiency), the immune system cannot mount adequate responses to pathogens; patients develop recurrent, severe, or opportunistic infections from childhood. In secondary immunodeficiency (HIV/AIDS, chemotherapy, immunosuppression), the defect is acquired; the person may have had normal immunity previously but loses it. Both result in increased susceptibility, but severely immunocompromised patients may not show classic fever because they lack an adequate inflammatory response. This explains why immunocompromised patients with serious infections may appear deceptively well while harboring severe infection, requiring vigilant monitoring.

Type II hypersensitivity involves IgG or IgM antibodies binding to antigens on a person's own cells, leading to complement-mediated destruction or phagocytosis. In ABO transfusion incompatibility, the recipient's pre-existing natural IgM antibodies (to the donor's red cell antigens) bind RBCs, activate complement, and cause hemolysis (rupture). This explains why blood type matching is absolutely critical before transfusion and why ABO incompatibility causes immediate, life-threatening reactions while Rh incompatibility causes delayed hemolytic disease of the newborn in Rh-negative mothers carrying Rh-positive babies.

In Type III hypersensitivity, antigen-antibody complexes form in the bloodstream and deposit in blood vessel walls, particularly in kidneys, joints, and skin. Complement activation follows, recruiting neutrophils and causing inflammation and tissue damage. Post-streptococcal glomerulonephritis is a classic example: Streptococcus pyogenes infection triggers antibody production; immune complexes deposit in the glomerulus; inflammation and proliferation damage the nephron; proteinuria and hematuria result. This explains why kidney function tests are monitored after severe streptococcal infection and why immunosuppression may be needed for severe Type III hypersensitivity.

In Type IV hypersensitivity, sensitized T lymphocytes recognize antigen and release cytokines that recruit macrophages; inflammation develops over 24–72 hours. The purified protein derivative (PPD) tuberculin skin test uses this mechanism: tuberculosis-sensitized T cells recognize PPD, recruit macrophages, and produce localized induration (hardness) at 48–72 hours. A positive test (≥5–15 mm depending on risk) indicates TB sensitization but not necessarily active disease. This explains why the PPD result is read at 48–72 hours (not immediately), why anergy (inability to mount PPD response) can occur in immunocompromised patients, and why TB disease requires 6+ months of anti-TB therapy.

During pregnancy, maternal IgG crosses the placenta and protects the fetus and newborn for the first few months of life (natural passive immunity). Through breast milk, maternal IgA protects the infant's mucous membranes (particularly against enteric and respiratory pathogens). However, these maternal antibodies gradually degrade over weeks to months, and the infant cannot yet mount an adequate active immune response. This is why infant vaccination schedules begin at 6 weeks of age and are spaced to build immunity as maternal antibodies wane. This explains why timing of vaccinations matters and why some antibiotics given to nursing mothers can affect the infant's immune system development.