NLE Immune System & Immunologic Disorders Reviewer 2026

Answer: C. Natural passive immunity

Step 1 — Ask: Did the infant's own immune system make these antibodies? No — they were transferred from the mother, so this is PASSIVE immunity. Step 2 — Ask: Was a medical intervention used? No — placental transfer is a natural biological process, so this is NATURAL. Step 3 — Therefore, this is natural passive immunity. The key feature: it is immediate but temporary because no immune memory was created. Step 4 — Why the others are wrong: Natural active = body makes its own antibodies after real infection (e.g., baby gets measles and recovers). Artificial active = body makes antibodies after a vaccine. Artificial passive = ready-made antibodies given via injection (e.g., HBIG, tetanus immunoglobulin).

Answer: D. IgE

Step 1 — IgE is the antibody class specifically associated with type I (immediate/anaphylactic) hypersensitivity. Step 2 — On first exposure to an allergen, B cells produce IgE, which binds to receptors on mast cells and basophils (sensitization). Step 3 — On re-exposure, the allergen cross-links the IgE on mast cells, triggering degranulation and release of histamine and other mediators — causing allergy symptoms. Step 4 — Why the others are wrong: IgG is the most abundant and crosses the placenta. IgM is the first antibody produced in acute infection. IgA is found in secretions like saliva and breast milk. None of these bind mast cells to trigger allergy.

Answer: D. Type IV — Delayed

Step 1 — Remember the mnemonic ACID: Type I = Anaphylactic (IgE), Type II = Cytotoxic (IgG/IgM), Type III = Immune complex (IgG/IgM complexes), Type IV = Delayed (T-cell mediated). Step 2 — Types I, II, and III are all antibody-mediated — they involve immunoglobulins produced by B cells. Step 3 — Type IV is unique: it is mediated by sensitized T lymphocytes, not antibodies. T cells recognize the antigen and release cytokines that recruit macrophages, causing inflammation 24–72 hours later — hence 'delayed.' Step 4 — Classic examples of Type IV: PPD/Mantoux tuberculin skin test reaction, contact dermatitis (e.g., from nickel or rubber), and transplant rejection. Step 5 — Key NLE point: The 24–72 hour delay distinguishes Type IV from the rapid (minutes) Type I reaction.

Answer: C. Epinephrine 0.3–0.5 mg IM (1:1000)

Step 1 — Anaphylaxis is a life-threatening emergency. Using Maslow's hierarchy, airway and circulation (physiologic survival needs) are top priority. Step 2 — Epinephrine is THE first-line, life-saving drug for anaphylaxis. It causes vasoconstriction (raises blood pressure), bronchodilation (opens the airway), and reduces laryngeal edema. Step 3 — The correct route is INTRAMUSCULAR (IM), preferably in the anterolateral thigh (vastus lateralis muscle). The correct concentration is 1:1000 (1 mg/mL). Adult dose: 0.3–0.5 mg IM. Step 4 — Why the others are wrong: Diphenhydramine (antihistamine) and hydrocortisone (steroid) are adjuncts — they act too slowly to reverse life-threatening laryngeal edema and shock. Salbutamol helps bronchospasm but does not treat shock or laryngeal edema. Step 5 — Critical NLE distinction: 1:1000 IM is for anaphylaxis; 1:10,000 IV is only for cardiac arrest.

Answer: B. Type II — Cytotoxic

Step 1 — Use the ACID mnemonic: Type I = Anaphylactic, Type II = Cytotoxic, Type III = Immune complex, Type IV = Delayed. Step 2 — In a hemolytic transfusion reaction, the recipient's IgG or IgM antibodies recognize foreign antigens on the donor's red blood cells and destroy them (cell lysis via complement). This is classic Type II — antibodies attack antigens ON a cell surface, leading to cell destruction (cytotoxicity). Step 3 — Other Type II examples: Rh incompatibility in newborns, autoimmune hemolytic anemia, myasthenia gravis, Graves disease, immune thrombocytopenia. Step 4 — Why the others are wrong: Type I involves IgE and mast cells. Type III involves immune complexes depositing in tissues (e.g., SLE, glomerulonephritis). Type IV involves T cells with a 24–72 hour delay.

Answer: B. Patients with spina bifida

Step 1 — Latex allergy develops through repeated exposure to latex. Patients with spina bifida require multiple surgeries and urinary catheterizations from birth, involving extensive contact with latex gloves and catheters. Step 2 — This repeated mucosal and skin exposure to latex proteins sensitizes the immune system over time, leading to IgE-mediated (Type I) latex allergy. Step 3 — Other high-risk groups: healthcare workers (frequent glove use), workers with heavy glove exposure (e.g., factory workers), and patients with a history of multiple surgeries. Step 4 — An important associated finding: latex-food cross-reactivity — patients with latex allergy may also react to banana, avocado, kiwi, and chestnut, because these foods share proteins similar to latex. Step 5 — Nursing implication: identify latex-sensitive patients on admission and provide a fully latex-free environment.

Answer: B. IgM

Step 1 — IgM is the first antibody class produced during a PRIMARY (initial) immune response to a new infection. Elevated IgM in the blood indicates a recent or active infection. Step 2 — IgM is the largest immunoglobulin — it is a pentamer (5 antibody units joined together). Step 3 — IgM does NOT cross the placenta (it is too large). This is clinically significant: if IgM is found in a newborn's blood, it means the baby made its own antibodies — suggesting a congenital infection (e.g., congenital rubella, syphilis, CMV). Step 4 — Why the others are wrong: IgG is the most abundant and is produced in the secondary (memory) response; IgG crosses the placenta. IgA is found in secretions. IgE mediates allergic reactions.

Answer: B. Anterolateral thigh (vastus lateralis)

Step 1 — For anaphylaxis, epinephrine 1:1000 is given intramuscularly (IM) into the anterolateral thigh (outer mid-thigh / vastus lateralis muscle). Step 2 — The anterolateral thigh is preferred because it has a rich blood supply, allowing for rapid absorption of epinephrine into the systemic circulation — faster than the deltoid. Step 3 — This is also the site used for epinephrine auto-injectors (e.g., EpiPen). The thigh can be injected even through clothing in an emergency. Step 4 — Why the others are wrong: The deltoid is acceptable for vaccines but is not the preferred site for anaphylaxis epinephrine — slower absorption. The gluteal site has variable absorption. IV push of 1:1000 is dangerous and not indicated for anaphylaxis (only 1:10,000 IV is used in cardiac arrest). Step 5 — Adult dose: 0.3–0.5 mg IM; Pediatric dose: 0.01 mg/kg IM up to 0.3 mg.

Answer: C. Perform meticulous hand hygiene before and after all patient contact

Step 1 — An immunocompromised patient has a deficient immune response and cannot fight infections effectively. Protection from infection is the top priority nursing goal. Step 2 — Hand hygiene is the single most effective measure to prevent healthcare-associated infections. The WHO's 5 Moments for Hand Hygiene applies strictly in caring for immunocompromised patients. Step 3 — Other protective (neutropenic) precautions include: private room, no raw fruits or vegetables (may harbor microorganisms), no fresh flowers or standing water (can harbor Pseudomonas and mold), limit visitors with infections. Step 4 — Why the others are wrong: Live vaccines (e.g., live attenuated influenza vaccine) are CONTRAINDICATED in significant immunodeficiency — the weakened pathogen can cause actual infection. Fresh flowers harbor mold spores. Shared communal areas expose the patient to pathogens. Step 5 — This aligns with NANDA nursing diagnosis: Risk for Infection related to immunosuppression.

Answer: D. Artificial active immunity

Step 1 — Ask: Is this ACTIVE or PASSIVE? The student's own immune system produced antibodies in response to the vaccine antigen — this is ACTIVE immunity. Memory cells were formed, so protection is long-lasting. Step 2 — Ask: Is it NATURAL or ARTIFICIAL? The vaccine is a human-made (artificial) medical product administered intentionally. It is NOT a natural infection. Step 3 — Therefore: ARTIFICIAL ACTIVE immunity. Step 4 — This is the same category as all vaccines: MMR, tetanus toxoid, BCG, DPT, OPV, HiB — all produce artificial active immunity because the body actively produces its own antibodies after receiving the vaccine. Step 5 — Compare: If the student was actually infected with Hepatitis B and recovered, that would be NATURAL ACTIVE immunity. If the student received Hepatitis B Immunoglobulin (HBIG), that would be ARTIFICIAL PASSIVE immunity.

Answer: B. Systemic Lupus Erythematosus (SLE)

Step 1 — Identify the hallmark finding: A rash across the cheeks and bridge of the nose that spares the nasolabial folds is called the 'butterfly' or malar rash. Step 2 — Link to disease: The malar rash is the classic hallmark of SLE and is caused by immune-complex (Type III hypersensitivity) deposition in the skin. Step 3 — Rule out other options: Scleroderma causes tight, hardened skin — not a butterfly rash. Sjögren's presents with dry eyes and dry mouth. Rheumatoid arthritis primarily affects joints without this skin pattern. Step 4 — Clinical pearl: The fact that the rash spares the nasolabial folds is a key distinguishing detail that points specifically to SLE's malar rash.

Answer: C. Antinuclear antibody (ANA)

Step 1 — Understand the question: It asks for the most SENSITIVE test, meaning the test that is positive in almost all SLE patients. Step 2 — Key fact: ANA is positive in nearly 95–99% of SLE patients, making it the best screening test. Step 3 — Distinguish from specific tests: Anti-dsDNA and anti-Sm are highly SPECIFIC for SLE (they point strongly to SLE when positive), but they are not present in all patients, so they are less sensitive. Step 4 — Rule out CRP: CRP is a general marker of inflammation; it is not specific or highly sensitive for SLE. Step 5 — Remember: Sensitivity = good for screening (few false negatives); Specificity = good for confirming (few false positives). ANA = sensitive screening tool; anti-dsDNA and anti-Sm = specific confirmatory tools.