NLE Immune System & Immunologic Disorders — Autoimmune Disorders and HIV/AIDSRevision Notes

Exam Tips

• NLE questions often test: 'Which type of immunity has memory?' — Answer: Adaptive immunity.
• If a question asks what provides IMMEDIATE protection without prior exposure, the answer is innate immunity.
• Remember: B cells = Antibodies (B for 'Both' humoral and B cells); T cells = Cell-mediated (T for 'Thymus').
• CD4 helper T cells are the cells DESTROYED by HIV — this is why HIV leads to immunodeficiency.

Key Points

• Immunity is the body's ability to resist and defend against foreign substances called antigens.
• Innate (natural, nonspecific) immunity is present from birth. It responds the same way to any invader and has NO memory. Components include skin and mucous membranes, phagocytes (neutrophils, macrophages), the complement system, and the inflammatory response.
• Adaptive (acquired, specific) immunity is antigen-specific, develops over time, and creates MEMORY so subsequent responses are faster and stronger.
• Adaptive immunity has two arms: HUMORAL immunity (B lymphocytes produce antibodies/immunoglobulins) and CELL-MEDIATED immunity (T lymphocytes — CD4 helper cells and CD8 cytotoxic cells).
• The first line of defense is physical barriers (skin, mucous membranes). The second line is innate cellular responses. The third line is adaptive immunity.
• Phagocytosis: neutrophils are the FIRST responders; macrophages arrive later and present antigens to T cells (antigen-presenting cells, APCs).
• CD4+ (helper T cells) coordinate the immune response by activating B cells and cytotoxic T cells via cytokines.
• CD8+ (cytotoxic T cells) directly kill virus-infected cells and tumor cells.
• B cells differentiate into plasma cells that secrete antibodies (immunoglobulins), and memory B cells for future rapid response.

Definitions

Section Title

Overview of Immunity: Innate vs. Adaptive

Common Mistakes

• Confusing innate immunity (nonspecific, no memory) with adaptive immunity (specific, has memory).
• Thinking that all immune responses are adaptive — innate immunity acts FIRST and does not require prior exposure.
• Confusing B lymphocytes (humoral/antibody-mediated) with T lymphocytes (cell-mediated).
• Forgetting that phagocytes (neutrophils, macrophages) are part of INNATE immunity, not adaptive.

Exam Tips

• High-yield: 'Which immunoglobulin crosses the placenta?' — IgG only.
• High-yield: 'Which immunoglobulin is elevated FIRST in an acute infection?' — IgM.
• High-yield: 'Which immunoglobulin mediates anaphylaxis?' — IgE.
• High-yield: 'Which immunoglobulin is found in breast milk?' — IgA (secretory IgA in colostrum).
• Use the mnemonic GAMED: IgG=most abundant/placenta, IgA=secretions, IgM=first/largest, IgE=allergy, IgD=B-cell receptor.

Key Points

• IgG: Most ABUNDANT immunoglobulin (75–80% of serum immunoglobulins). The ONLY one that crosses the placenta to give the newborn passive immunity. Responsible for the SECONDARY (memory/booster) response. Also mediates Type II and III hypersensitivity.
• IgM: The LARGEST immunoglobulin. The FIRST antibody produced in a PRIMARY (acute) infection — elevated IgM = recent/acute infection. Does NOT cross the placenta. Important in ABO blood group reactions.
• IgA: Found in SECRETIONS — saliva, tears, colostrum and breast milk, bronchial mucus, intestinal secretions. Protects mucosal surfaces. IgA in breast milk provides passive immunity to breastfed infants. Selective IgA deficiency is the most common primary immunodeficiency.
• IgE: Mediates ALLERGIC and ANAPHYLACTIC reactions (Type I hypersensitivity). Binds mast cells and basophils. Normal serum levels are very low, but elevated in atopic individuals and parasitic infections.
• IgD: Present on the surface of B lymphocytes as a receptor. Its clinical role is least understood; not a common NLE focus.
• Memory device: GAMED — IgG (most abundant), IgA (secretions), IgM (first/largest), IgE (allergy), IgD (B-cell receptor).

Definitions

Section Title

The Five Immunoglobulins (IgG, IgM, IgA, IgE, IgD)

Common Mistakes

• Stating that IgM crosses the placenta — WRONG. Only IgG crosses the placenta.
• Confusing IgM (first antibody in acute infection) with IgG (secondary response/memory antibody).
• Saying IgA is the most abundant — IgG is the most abundant in serum; IgA is the most abundant in secretions.
• Forgetting that IgE is involved in BOTH allergy AND parasitic infections (elevated IgE is not always allergy).

Exam Tips

• Classic NLE question pattern: 'A patient who never received any vaccines is exposed to hepatitis B. What should be given?' — HBIG (artificial passive, immediate) PLUS hepatitis B vaccine (artificial active, for long-term) at a different site.
• Another classic: 'A child survived chickenpox. What type of immunity does she now have?' — Natural active immunity.
• Remember: Passive = borrowed = temporary = no memory. Active = self-made = lasting = memory.
• Philippine EPI vaccines (BCG, OPV, DPT, hepatitis B, measles) all = ARTIFICIAL ACTIVE immunity.

Key Points

• The KEY distinction: ACTIVE immunity = the person's OWN immune system makes antibodies → slow onset, LONG-LASTING (months to years) because memory cells are created. PASSIVE immunity = ready-made antibodies are GIVEN to the person → IMMEDIATE onset, but SHORT-LIVED (weeks to months) because no memory is created and borrowed antibodies are eventually catabolized.
• NATURAL ACTIVE immunity: Body produces antibodies after surviving an actual infection. Example: immunity after having chickenpox, measles, or mumps. Very long-lasting, often lifelong.
• ARTIFICIAL ACTIVE immunity: Body produces antibodies after receiving a VACCINE (made of attenuated/killed antigen or toxoid). Examples: MMR, hepatitis B, tetanus toxoid, BCG, OPV. Slow to develop; requires 2–4 weeks; may need boosters.
• NATURAL PASSIVE immunity: Ready-made antibodies transferred from MOTHER to CHILD. Via PLACENTA (IgG) during the third trimester, or via BREAST MILK/COLOSTRUM (secretory IgA). Temporary — lasts approximately 3–6 months in the newborn.
• ARTIFICIAL PASSIVE immunity: Ready-made antibodies given as an INJECTION (immune serum/globulin). Used for IMMEDIATE post-exposure prophylaxis. Examples: tetanus immunoglobulin (TIG), hepatitis B immunoglobulin (HBIG), rabies immunoglobulin (RIG), antivenom (for snake bite), anti-D immunoglobulin (RhoGAM for Rh incompatibility).
• In the Philippine Expanded Program on Immunization (EPI), all childhood vaccines confer ARTIFICIAL ACTIVE immunity.
• When a mother who had measles before feeds her baby, the baby gets NATURAL PASSIVE immunity through breast milk (IgA).
• When a health worker is stuck by a needle from an HBsAg-positive patient and is given HBIG, that is ARTIFICIAL PASSIVE immunity — for immediate short-term protection.

Definitions

Section Title

Types of Acquired Immunity: Active vs. Passive, Natural vs. Artificial

Common Mistakes

• Saying vaccines provide PASSIVE immunity — WRONG. Vaccines provide ARTIFICIAL ACTIVE immunity.
• Confusing tetanus toxoid (TIG) with tetanus vaccine — TIG gives PASSIVE (immediate, short-lived) protection; tetanus toxoid gives ACTIVE protection.
• Thinking placental transfer gives the baby ACTIVE immunity — it is NATURAL PASSIVE immunity.
• Forgetting that passive immunity is SHORT-LIVED because no memory cells are created.
• Mixing up the timing: active immunity takes WEEKS to develop; passive immunity works IMMEDIATELY.

Exam Tips

• Use ACID: I=Anaphylactic(IgE), II=Cytotoxic(IgG/IgM, cells), III=Immune complex(deposits), IV=Delayed(T-cells, 24-72h).
• ABO transfusion reaction = TYPE II (antibody attacks cells). This is different from transfusion-related anaphylaxis (TYPE I).
• PPD/Mantoux positive at 48–72 hours = TYPE IV. This is textbook.
• Graft rejection = TYPE IV. Contact dermatitis = TYPE IV. Remember: both are T-cell mediated.
• SLE = TYPE III (immune complex deposits in kidneys, joints, skin). RA = TYPE III.
• Myasthenia gravis and Graves disease = TYPE II (antibodies block or stimulate receptors on cell surfaces).

Key Points

• Hypersensitivity is an EXAGGERATED or inappropriate immune response to an antigen that causes TISSUE DAMAGE. The Gell and Coombs classification identifies four types.
• MEMORY MNEMONIC — ACID: Type I = Anaphylactic/Allergic, Type II = Cytotoxic, Type III = Immune complex, Type IV = Delayed (cell-mediated).
• Types I, II, and III are ANTIBODY-MEDIATED (humoral) — they generally occur rapidly (minutes to hours). Type IV is T-CELL mediated and is DELAYED (24–72 hours).
• TYPE I (Anaphylactic): Mediated by IgE. First exposure = sensitization (IgE binds to mast cells and basophils). Re-exposure = antigen cross-links IgE → mast cell degranulation → histamine, leukotrienes, prostaglandins released. Causes vasodilation, increased capillary permeability, bronchoconstriction. Occurs within MINUTES. Examples: anaphylaxis, allergic rhinitis, allergic asthma, urticaria, food allergy, drug allergy (penicillin), latex allergy (immediate form), insect venom allergy.
• TYPE II (Cytotoxic): Mediated by IgG or IgM antibodies directed against antigens on the SURFACE of the body's OWN CELLS. Complement activation or phagocytosis destroys the cell. Examples: ABO-incompatible blood transfusion reaction (classic), Rh incompatibility/hemolytic disease of the newborn (HDN), autoimmune hemolytic anemia, immune thrombocytopenic purpura (ITP), Goodpasture syndrome (anti-GBM antibodies attack the kidney and lung), myasthenia gravis (anti-AChR antibodies), Graves disease (anti-TSH receptor antibodies).
• TYPE III (Immune Complex): Antigen-antibody (immune) complexes form in circulation and DEPOSIT in tissues and vessel walls. Complement is activated, causing inflammation and tissue destruction. Examples: Systemic Lupus Erythematosus (SLE), rheumatoid arthritis (RA), post-streptococcal acute glomerulonephritis, serum sickness, Arthus reaction.
• TYPE IV (Delayed/Cell-Mediated): The ONLY type NOT mediated by antibodies. Sensitized T LYMPHOCYTES react with antigen, releasing cytokines that recruit macrophages, producing inflammation over 24–72 HOURS. Examples: Tuberculin (PPD/Mantoux) skin test reaction (classic example), contact dermatitis (poison ivy, nickel, cosmetics, latex delayed form), transplant/graft rejection, granulomatous diseases (tuberculosis, sarcoidosis, leprosy).
• A Mantoux test that is positive at 48–72 hours demonstrates Type IV hypersensitivity — this is a NORMAL and EXPECTED mechanism of the test, not an allergy emergency.
• The ABO transfusion reaction is the classic Type II example: recipient has IgM antibodies (anti-A or anti-B) that attack the donor red blood cells → intravascular hemolysis.

Definitions

Section Title

The Four Types of Hypersensitivity Reactions (ACID Mnemonic)

Common Mistakes

• Saying the Mantoux/PPD test is a Type I reaction — it is TYPE IV (delayed, 48–72 hours, T-cell mediated). A wheal-and-flare within minutes would be Type I.
• Forgetting that Type IV is the ONLY non-antibody-mediated hypersensitivity — it is T-cell mediated.
• Confusing Type II (cell-surface antibodies) with Type III (soluble immune complexes). Type II targets antigens ON cells; Type III involves complexes DEPOSITING in tissues.
• Listing SLE under Type II — SLE involves immune complex DEPOSITION, making it Type III.
• Thinking transplant rejection is Type I — transplant rejection is Type IV (cell-mediated T lymphocytes).

Exam Tips

• NLE frequently tests: 'Before administering any medication, what should the nurse do first?' — Check for ALLERGIES.
• Diphenhydramine causes sedation — advise patients NOT to drive; this is a common patient teaching question.
• Corticosteroid teaching: do not stop abruptly, take with food, monitor blood glucose (hyperglycemia is a side effect).
• Skin testing must always be done with emergency equipment nearby — this is a patient safety principle under RA 9173.
• Second-generation antihistamines (cetirizine, loratadine, fexofenadine) are preferred for daytime use due to less sedation.

Key Points

• Allergy is a Type I hypersensitivity to an ordinarily harmless environmental antigen (allergen). Common allergens: pollen, dust mites, mold, animal dander, foods (peanuts, shellfish, tree nuts, eggs, milk), insect venom, medications (penicillin is the classic drug allergen), and latex.
• CLINICAL MANIFESTATIONS: Respiratory (sneezing, rhinorrhea, nasal congestion, wheezing, cough), Skin (urticaria/hives, pruritus/itching, erythema, angioedema — swelling of lips, tongue, face, eyelids), Eyes (itching, tearing, allergic conjunctivitis), GI (nausea, vomiting, cramping, diarrhea — common in food allergy).
• NURSING ASSESSMENT: Always take a thorough ALLERGY HISTORY — specific allergen, timing of reaction, prior reactions and their severity, cross-reactive substances, and current medications. Always ask about drug allergies BEFORE administering any medication (this is a nursing standard under RA 9173).
• SKIN TESTING (scratch, prick, or intradermal): A WHEAL-AND-FLARE within 15–20 minutes indicates IgE-mediated sensitivity. EMERGENCY EQUIPMENT (epinephrine, oxygen, IV access) must be available at all times during skin testing because of the risk of anaphylaxis.
• DIAGNOSTIC TESTS: Serum total IgE (elevated in atopic individuals), specific IgE (RAST/ImmunoCAP — identifies which specific allergen the person is sensitized to), CBC with differential (eosinophilia supports allergic process), nasal smear for eosinophils.
• ANTIHISTAMINES: Block H1 receptors, reducing histamine-mediated symptoms (itch, rhinorrhea, urticaria). First-generation: diphenhydramine (Benadryl) — causes SEDATION and ANTICHOLINERGIC effects (dry mouth, urinary retention, blurred vision); caution when driving or operating machinery, and in older adults. Second-generation: cetirizine (Zyrtec), loratadine (Claritin), fexofenadine (Allegra) — LESS sedating, preferred for daytime use.
• CORTICOSTEROIDS: Prednisone (systemic), fluticasone, budesonide (intranasal). Reduce inflammation. Used for moderate-to-severe or chronic allergy. NEVER stop systemic corticosteroids ABRUPTLY — taper slowly to prevent adrenal crisis.
• MAST CELL STABILIZERS: Cromolyn sodium — prevents degranulation; must be used PROPHYLACTICALLY (before exposure), not for acute symptoms.
• LEUKOTRIENE MODIFIERS: Montelukast (Singulair) — used prophylactically for allergic asthma and rhinitis.
• DECONGESTANTS: Pseudoephedrine — relieves nasal congestion by vasoconstriction; AVOID in hypertension, heart disease, hyperthyroidism, and pregnancy.
• ALLERGEN IMMUNOTHERAPY (desensitization): Gradual exposure to increasing amounts of the allergen via subcutaneous injections to reduce sensitivity. Patients must be observed for 20–30 minutes after each injection; emergency equipment must be available.

Definitions

Section Title

Allergic Reactions: Assessment, Diagnosis, and Pharmacologic Management

Common Mistakes

• Giving diphenhydramine FIRST in anaphylaxis — EPINEPHRINE is always first; antihistamines are adjuncts.
• Stopping corticosteroids abruptly — must be TAPERED to prevent adrenal insufficiency.
• Giving cromolyn AFTER symptoms start — it is a PROPHYLACTIC agent only, not for acute attacks.
• Forgetting to have epinephrine available during skin testing — anaphylaxis can be triggered.
• Not asking about penicillin allergy — cross-reactivity with cephalosporins (especially first-generation) is clinically important.

Formulas

Exam Tips

• MOST TESTED: 'What is the PRIORITY nursing action/drug for anaphylaxis?' — Administer EPINEPHRINE (IM, 0.3–0.5 mg, 1:1000, anterolateral thigh).
• Airway obstruction (laryngeal edema) is the #1 cause of death in anaphylaxis — always prioritize airway.
• Remember the concentrations: 1:1000 (1 mg/mL) = IM for anaphylaxis. 1:10,000 (0.1 mg/mL) = IV for cardiac arrest.
• Biphasic reaction is tested: 'The patient seems fine after treatment. What should the nurse do?' — Continue monitoring for at least 4–8 hours.
• Patient teaching questions: Carry EpiPen, wear medical-alert bracelet, avoid known allergen, seek ER after every EpiPen use.
• Sense of impending doom is an early, classic subjective symptom of anaphylaxis — take it seriously.

Key Points

• Anaphylaxis is a SEVERE, RAPID, SYSTEMIC Type I hypersensitivity reaction that is LIFE-THREATENING. It represents the most extreme end of the allergic spectrum. Onset is within SECONDS TO MINUTES of exposure to the trigger.
• PATHOPHYSIOLOGY: Massive IgE-triggered mast cell degranulation → widespread vasodilation + increased vascular permeability (distributive/vasogenic shock) → profound HYPOTENSION + BRONCHOCONSTRICTION + LARYNGEAL EDEMA. Laryngeal edema is the LEADING CAUSE OF DEATH in anaphylaxis.
• COMMON TRIGGERS: Medications (penicillin, sulfonamides, aspirin, NSAIDs, contrast media), foods (peanuts, shellfish, tree nuts, eggs), insect stings (bee/wasp venom), latex, blood/blood products, vaccines (rarely), immunotherapy injections.
• EARLY MANIFESTATIONS: Pruritus (itching), flushing, urticaria, angioedema, sense of impending doom (a key early subjective sign), anxiety.
• PROGRESSIVE MANIFESTATIONS — ABC approach: AIRWAY: throat tightness, hoarseness, STRIDOR (high-pitched inspiratory sound indicating upper airway narrowing), laryngeal edema. BREATHING: wheezing, dyspnea, bronchospasm, chest tightness (lower airway). CIRCULATION: tachycardia, HYPOTENSION, dizziness, syncope, cardiovascular collapse (shock).
• BIPHASIC REACTION: A second wave of anaphylactic symptoms can occur 1–8 hours (up to 72 hours) after the initial reaction even with adequate treatment — reason why patients must be observed in a healthcare setting for at least 4–8 hours (some guidelines recommend 24 hours for severe reactions).
• PRIORITY NURSING ACTION — THE FIVE-STEP EMERGENCY RESPONSE: (1) EPINEPHRINE FIRST — the ONLY life-saving first-line drug. (2) Maintain AIRWAY — oxygen, positioning, prepare for intubation. (3) REMOVE or STOP the trigger. (4) POSITION the patient. (5) IV ACCESS and FLUIDS.
• EPINEPHRINE DOSING (CRITICAL NLE FACT): Adult: 0.3–0.5 mg of 1:1000 (1 mg/mL) solution given INTRAMUSCULARLY into the ANTEROLATERAL THIGH (vastus lateralis muscle). May repeat every 5–15 minutes. Pediatric: 0.01 mg/kg IM, maximum 0.3 mg. 1:1000 = IM for anaphylaxis. 1:10,000 = IV for cardiac arrest. DO NOT CONFUSE.
• Why anterolateral thigh? Fastest absorption due to greater muscle mass and vascularity compared to the deltoid.
• POSITIONING: Supine with legs ELEVATED (Trendelenburg-like) to improve venous return and perfusion — UNLESS respiratory distress is present, in which case allow the patient to sit upright (Semi-Fowler's) to ease breathing.
• ADJUNCT MEDICATIONS (secondary, not first-line): Diphenhydramine (Benadryl) IV/IM — H1 antihistamine for urticaria; Ranitidine or famotidine — H2 blocker; Hydrocortisone or methylprednisolone IV — corticosteroid to prevent biphasic reaction (takes hours to work); Nebulized salbutamol (albuterol) — for persistent bronchospasm. NONE of these replaces epinephrine.
• HIGH-FLOW OXYGEN via face mask is given to all patients in anaphylaxis.
• IV access and RAPID isotonic crystalloid infusion (normal saline/lactated Ringer's) for hypotension.
• Monitor: vital signs every 5 minutes, oxygen saturation (SpO2), cardiac rhythm (tachycardia, arrhythmias), mental status, urine output.

Definitions

Section Title

Anaphylaxis: Recognition, Emergency Management, and Patient Teaching

Common Mistakes

• Giving diphenhydramine (Benadryl) FIRST in anaphylaxis — EPINEPHRINE is ALWAYS first. Antihistamines are far too slow.
• Giving epinephrine IV (1:1000) for anaphylaxis — 1:1000 is given IM. IV epinephrine in 1:10,000 concentration is for cardiac arrest.
• Injecting epinephrine in the DELTOID instead of the anterolateral thigh — thigh is preferred for faster absorption.
• Not watching for biphasic reaction — patients must be observed for at least 4–8 hours after anaphylaxis.
• Not elevating the legs in anaphylactic shock (unless respiratory distress is present).
• Thinking corticosteroids are the priority drug — they take hours to work and are only adjuncts.
• Not instructing the patient to carry an epinephrine auto-injector after discharge.

Exam Tips

• High-yield: 'A patient with spina bifida is scheduled for surgery. What should the nurse prioritize?' — Prepare a LATEX-FREE environment and schedule as FIRST case of the day.
• High-yield: 'A healthcare worker develops eczema on the hands after wearing latex gloves. What type of reaction is this?' — Type IV (delayed hypersensitivity, contact dermatitis).
• Remember the cross-reactive foods: BANANA, AVOCADO, KIWI, CHESTNUT.
• If a latex-allergic patient develops urticaria and wheezing in the OR → Type I anaphylaxis → give EPINEPHRINE immediately.

Key Points

• Latex allergy is an important occupational health hazard in Philippine healthcare settings due to widespread glove use. Natural rubber latex comes from the Hevea brasiliensis tree.
• TWO TYPES of latex reactions: TYPE IV (Delayed Contact Dermatitis) — most common form; T-cell-mediated eczematous skin reaction to chemicals added during rubber manufacturing (thiurams, carbamates); appears 24–48 hours after contact; presents as red, itchy, blistering rash. TYPE I (IgE-mediated Immediate Reaction) — the DANGEROUS form; IgE-mediated reaction to latex proteins; can cause urticaria, rhinitis, asthma, and progress to ANAPHYLAXIS; occurs within minutes of contact.
• HIGH-RISK GROUPS for latex allergy: (1) Healthcare workers (repeated occupational glove exposure), (2) Patients with SPINA BIFIDA — highest risk; repeated bladder catheterizations and surgeries since infancy, (3) Patients with multiple prior surgeries, (4) Rubber industry workers, (5) Individuals with food allergies to BANANA, AVOCADO, KIWI, and CHESTNUT (latex-food syndrome / cross-reactivity). Memory tip: Banana, Avocado, Kiwi, Chestnut = BAKC or think 'BACK' plus kiwi.
• LATEX IS FOUND IN: surgical and examination gloves, catheters, IV tubing ports, tourniquets, blood pressure cuffs, electrode pads, anesthesia equipment, dental dams, and some adhesive tape.
• NURSING MANAGEMENT: (1) Identify at-risk patients on ADMISSION using a screening tool; (2) Document latex allergy prominently in the chart, wristband, and medication administration record (MAR); (3) Establish a LATEX-FREE ENVIRONMENT — use non-latex (vinyl, nitrile, or neoprene) gloves and latex-free equipment; (4) Schedule latex-sensitive patients as the FIRST CASE OF THE DAY in the operating room (OR) or procedure rooms to minimize airborne latex particles from previous glove use; (5) Keep emergency anaphylaxis supplies (epinephrine, oxygen) readily available.
• Teach patients to inform ALL healthcare providers (dentists, doctors, nurses) of latex allergy and to wear a medical-alert bracelet.
• Latex-free carts/kits should be available in all Philippine hospital settings as part of patient safety protocols.

Definitions

Section Title

Latex Allergy

Common Mistakes

• Thinking all latex reactions are Type I — the most COMMON form is Type IV (delayed contact dermatitis); Type I is the DANGEROUS form.
• Forgetting that patients with SPINA BIFIDA are at the HIGHEST RISK for latex allergy.
• Not scheduling latex-allergic patients first in the OR — airborne latex particles from earlier glove use can trigger reactions.
• Forgetting the latex-food cross-reactivity: banana, avocado, kiwi, chestnut.

Exam Tips

• Classic NLE pattern: 'A patient undergoing chemotherapy has a temperature of 38.2°C. What is the priority nursing action?' — Report to physician immediately; this is a potential neutropenic fever emergency.
• Live vaccines contraindicated in immunodeficiency: MMR, varicella, yellow fever, oral typhoid, oral polio (OPV), BCG (active TB risk).
• SCID = Both B and T cells defective. Bruton's = B cells only. DiGeorge = T cells only (no thymus). Selective IgA = IgA only.
• HIV destroys CD4+ T-helper cells. AIDS is diagnosed when CD4 <200 cells/μL.
• IVIG infusion: start SLOW, monitor for chills, fever, headache, flushing; have epinephrine ready.

Key Points

• Immunodeficiency is a state of deficient immune function leaving the individual vulnerable to infections that a normal immune system would control. The hallmark is RECURRENT, SEVERE, or UNUSUAL infections.
• PRIMARY (CONGENITAL) IMMUNODEFICIENCY: Inherited genetic defects; present from birth. Rare. Key examples: SCID (Severe Combined Immunodeficiency) — the 'bubble boy' disorder; defect in BOTH B and T lymphocytes; profound susceptibility to all infections; treated with bone marrow transplant. Bruton Agammaglobulinemia (X-linked) — defect in B-cell maturation; no immunoglobulins; boys are affected; recurrent bacterial infections starting at ~6 months (after maternal IgG wanes). Selective IgA Deficiency — most common primary immunodeficiency; recurrent respiratory and GI infections. DiGeorge Syndrome — failure of thymus development; absent T-cells; susceptibility to viral and fungal infections.
• SECONDARY (ACQUIRED) IMMUNODEFICIENCY: MUCH more common; results from another condition, treatment, or factor. Major causes: HIV/AIDS (destroys CD4+ T-helper cells — the CLASSIC secondary immunodeficiency), malignancy (leukemia, lymphoma), chemotherapy and radiation therapy (suppress bone marrow), immunosuppressive medications (corticosteroids, cyclosporine, methotrexate), malnutrition and protein deficiency, splenectomy (increased risk for encapsulated bacteria: S. pneumoniae, H. influenzae, Neisseria), aging (immunosenescence), diabetes mellitus, renal failure, burns.
• HIV/AIDS: HIV selectively infects and destroys CD4+ T-helper lymphocytes. When CD4 count falls below 200 cells/μL, AIDS is diagnosed. Opportunistic infections (Pneumocystis jirovecii pneumonia/PCP, CMV retinitis, Candida, Toxoplasma, MAC) develop. Antiretroviral therapy (ART) is the cornerstone of management.
• NURSING MANAGEMENT FOR IMMUNODEFICIENCY: (1) PROTECTIVE (NEUTROPENIC) PRECAUTIONS: Private room preferred; meticulous hand hygiene (the single most important measure); limit visitors and exclude those with illness; avoid raw fruits, vegetables, and undercooked meat in severely neutropenic patients; no fresh flowers or standing water (Pseudomonas risk); monitor for infection signs. (2) Recognize that fever may be the ONLY sign of infection in an immunocompromised patient — report temperature ≥38°C (100.4°F) promptly. (3) LIVE VACCINES are CONTRAINDICATED in significant immunodeficiency (MMR, varicella, yellow fever, oral polio — can cause infection with the vaccine strain). Inactivated vaccines may be given. (4) IVIG (Intravenous Immunoglobulin) may be given for antibody deficiencies; infuse SLOWLY; monitor for infusion reactions (fever, chills, headache); have epinephrine available. (5) Nutritional support — adequate protein and micronutrients support immune function.
• In the Philippine healthcare context, HIV cases are rising among the youth and men who have sex with men (MSM). The DOH provides ARV therapy through treatment hubs. Nurses must maintain CONFIDENTIALITY per RA 8504 (Philippine AIDS Prevention and Control Act).
• Neutropenic precautions are standard of care in Philippine hospitals for patients undergoing chemotherapy; the oncology nurse must assess the absolute neutrophil count (ANC) and implement protective measures when ANC falls below 500 cells/μL (severe neutropenia).

Definitions

Section Title

Immunodeficiency: Primary and Secondary

Common Mistakes

• Giving LIVE vaccines to immunocompromised patients — live vaccines can cause actual infection (vaccine-strain disease) in immunodeficient patients.
• Thinking the only sign of infection in a neutropenic patient is fever — the fever may be low-grade or absent; any change in condition warrants prompt assessment.
• Confusing SCID (primary, genetic, both B and T cells) with AIDS (secondary, acquired, specifically CD4+ T cells).
• Allowing fresh flowers in a neutropenic patient's room — flowers carry Pseudomonas and mold spores.
• Not following confidentiality requirements for HIV-positive patients — RA 8504 mandates strict confidentiality.