Immune System & Immunology NCLEX Practice Questions

A CD4 count below 200 cells/mm3 both defines AIDS and is the threshold for starting primary prophylaxis against Pneumocystis pneumonia (PCP). Trimethoprim-sulfamethoxazole (TMP-SMX, Bactrim) is the first-line agent, so this is the anticipated order at a count of 180.

Isoniazid is used to treat latent tuberculosis infection and is guided by a positive screening test (interferon-gamma release assay or tuberculin skin test), not by a CD4 value, so it would not be started based on this count alone. Azithromycin prophylaxis against Mycobacterium avium complex is considered when the CD4 count falls below 50 cells/mm3; at 180 the client is above that threshold. Discontinuing antiretroviral therapy is never appropriate because ART is precisely what restores the CD4 count and suppresses viral replication; stopping it would deepen immunosuppression and promote resistance.

Clinical pearl: remember "200 = PCP, 50 = MAC." As the CD4 count drops, opportunistic-infection risk climbs and prophylaxis is layered in at those two cutoffs. Standard precautions apply to every client regardless of HIV status, and HIV-negative partners at ongoing risk may be offered pre-exposure prophylaxis (PrEP). Reinforce strict ART adherence, because consistent viral suppression is the single most important factor in preventing opportunistic infection.

This client is in anaphylaxis, a Type I (immediate, IgE-mediated) hypersensitivity reaction with airway compromise and shock. Intramuscular epinephrine given into the anterolateral thigh is the always-first-line, life-saving intervention. Epinephrine reverses the reaction through alpha-1 vasoconstriction (raising blood pressure and reducing mucosal edema) and beta-2 bronchodilation, and it stabilizes mast cells. It should be given immediately and can be repeated every 5 to 15 minutes as needed.

Diphenhydramine, an antihistamine, only blocks histamine at receptors, will not reliably reverse airway swelling, and does nothing for the bronchospasm or hypotension that kill in anaphylaxis; it is an adjunct given after epinephrine. Corticosteroids blunt the delayed, biphasic phase of the reaction but take hours to work, so they are never the first drug. Positioning and oxygen support the client, but a hypotensive client should be placed supine with the legs elevated, not in high Fowler's, which can worsen venous return and precipitate cardiovascular collapse; regardless, positioning does not substitute for epinephrine.

Clinical pearl: "Epi first, epi fast, epi in the thigh." The intramuscular route into the vastus lateralis gives the most reliable absorption. Delaying epinephrine to give antihistamines or steroids is a classic fatal error the NCLEX tests directly.

SLE is a chronic autoimmune disease marked by photosensitivity, so protecting the skin from ultraviolet light is central teaching. Applying broad-spectrum sunscreen, avoiding direct sun, and wearing protective clothing such as long sleeves and a wide-brimmed hat all reduce UV-triggered flares and the characteristic malar (butterfly) rash. Because both the disease and the immunosuppressive medications used to treat it raise infection risk, promptly reporting fever or other signs of infection is essential. Using mild soaps and avoiding harsh skin products helps protect fragile, inflamed skin.

Discontinuing corticosteroids as soon as symptoms improve is dangerous and incorrect: corticosteroids must be tapered under provider supervision, and abrupt cessation can cause a lupus flare and, potentially, adrenal insufficiency. Tanning beds emit ultraviolet radiation and would worsen, not improve, the rash and can trigger a systemic flare, so this instruction is unsafe.

Clinical pearl: think "SLE = Sun, Lupus, Exacerbation." UV light is one of the most common and controllable flare triggers, making daily sun protection a nonnegotiable part of the teaching plan. Also reinforce energy conservation for fatigue and adherence to prescribed immunomodulators such as hydroxychloroquine, which requires periodic eye exams.

A cholinergic crisis results from overmedication with cholinesterase inhibitors (such as pyridostigmine), causing excess acetylcholine at the neuromuscular junction and muscarinic overstimulation. The hallmark is the SLUDGE picture: salivation, lacrimation, urination, defecation, gastrointestinal cramping, and emesis, along with miosis and increased bronchial secretions. Excessive salivation, lacrimation, and abdominal cramping therefore point to a cholinergic crisis. Because more medication would worsen it, these clients need their cholinesterase inhibitor held and, potentially, atropine.

The other findings describe a myasthenic crisis, which is caused by undermedication or a trigger such as infection, stress, or surgery. Improvement in muscle strength after pyridostigmine, weakness that follows missed doses, and ptosis or dysphagia that resolve with a cholinesterase inhibitor all indicate too little acetylcholine effect; these clients need more medication, not less.

Both crises can compromise the diaphragm and airway, so the shared nursing priority is always monitoring respiratory status and being prepared to support ventilation. Historically edrophonium (Tensilon) was used to distinguish the two: strength improves in a myasthenic crisis and worsens in a cholinergic crisis. Clinical pearl: myasthenic crisis = "need more" (weakness from too little drug); cholinergic crisis = "too much" (wet, SLUDGE symptoms from too much drug).

Type IV hypersensitivity is a delayed, T-cell (cell-mediated) response that develops over 24 to 72 hours rather than minutes, and does not involve antibodies. Classic examples are contact dermatitis from poison ivy, latex, or nickel; the tuberculin (PPD) skin-test reaction; and transplant graft rejection. Poison-ivy contact dermatitis is therefore the correct Type IV example.

Anaphylaxis after a bee sting is Type I: an immediate, IgE-mediated reaction that causes mast-cell degranulation within minutes. A hemolytic reaction from ABO-incompatible blood is Type II (cytotoxic), in which IgG or IgM antibodies bind antigens on cell surfaces and trigger complement-mediated cell destruction. Serum sickness from circulating drug-antigen complexes is Type III (immune complex), where antigen-antibody complexes deposit in tissues and incite inflammation.

Clinical pearl for the four types: "ACID" helps — Type I Anaphylactic (immediate), Type II Cytotoxic, Type III Immune complex, Type IV Delayed. Remember that Types I through III are antibody-mediated and relatively fast, while Type IV is uniquely cell-mediated and delayed, which is why a PPD is read two to three days later.

Transplant recipients take immunosuppressants for the life of the graft to prevent rejection, so consistent dosing at the same time daily without skipping doses is critical; erratic drug levels invite acute rejection. Because these drugs deliberately suppress immunity, the client is highly vulnerable to infection: avoiding crowds and sick contacts and promptly reporting a fever of 100.4 F (38 C) or higher are essential, since fever may be the only early sign of infection or rejection. Grapefruit and grapefruit juice inhibit the CYP3A4 enzyme, raising tacrolimus and cyclosporine levels to toxic ranges, so they must be avoided.

Stopping the medications once the organ works well is incorrect and dangerous; discontinuation predictably triggers rejection, which for a kidney can be irreversible. Receiving live attenuated vaccines (such as MMR or varicella) is contraindicated in immunosuppressed clients because the weakened live organism can cause active disease; only non-live vaccines (for example, the inactivated influenza vaccine) are appropriate.

Clinical pearl: rejection comes in three timeframes — hyperacute (minutes to hours, preformed antibodies), acute (days to months, often reversible with increased immunosuppression), and chronic (months to years, gradual and irreversible). Because signs of rejection and infection overlap (fever, malaise, graft tenderness, rising creatinine for a kidney), any of these should be reported immediately. Also stress meticulous hand hygiene and food safety.

MMR is a live attenuated vaccine, so it is contraindicated in significantly immunocompromised clients because the weakened virus can replicate and cause disease. A client on high-dose corticosteroids after an organ transplant is immunosuppressed and should not receive it. Live-vaccine contraindications also include pregnancy, HIV with a CD4 count below 200 cells/mm3, active leukemia or lymphoma, and other primary or acquired immunodeficiencies.

The healthy 15-month-old is precisely the recommended age for the first MMR dose (12 to 15 months), so vaccination is appropriate and important. A 25-year-old woman who is not pregnant and lacks immunity is a good candidate; she should simply be counseled to avoid pregnancy for about one month afterward. A healthcare worker without evidence of measles immunity is specifically targeted for MMR to protect the worker and patients, and being an adult in a healthcare role is not a contraindication.

Clinical pearl: live vaccines — MMR, varicella, live attenuated influenza (nasal spray), rotavirus, and yellow fever — are the ones to withhold in pregnancy and immunosuppression. Clients with primary immunodeficiency should also avoid live vaccines. When in doubt, ask whether the vaccine is live: if it is, screen carefully for immunocompromise and pregnancy before administering.

Sustained viral suppression is the goal of ART. When a person maintains an undetectable viral load, they cannot sexually transmit HIV to partners — the evidence-based Undetectable = Untransmittable (U=U) concept endorsed by the CDC. Telling the client this is both accurate and motivating for adherence.

Saying the client is cured and can stop medication is false: ART suppresses viral replication but does not eradicate HIV, which persists in latent reservoirs. Stopping treatment allows the virus to rebound, the CD4 count to fall, and drug resistance to develop. Similarly, stopping and restarting the medication based on how the client feels is dangerous; intermittent adherence is a leading cause of treatment failure and resistance, so ART must be taken consistently every day for life. The statement that no precautions are needed for bloodborne exposure is incorrect: U=U applies to sexual transmission with sustained viral suppression, but standard precautions still apply to blood and body fluids for all clients, and the client should not share razors or needles.

Clinical pearl: the mantra is "adherence, adherence, adherence." Emphasize that lifelong, consistent ART keeps the viral load undetectable, preserves immune function, prevents opportunistic infections, and (via U=U) protects partners. Pre-exposure prophylaxis (PrEP) remains an option for HIV-negative partners at risk.

People with latex allergy can react to certain plant foods that share proteins with natural rubber latex, a phenomenon called latex-fruit syndrome. The foods most strongly associated with cross-reactivity are banana, avocado, kiwi, and chestnut; these should be highlighted for the client. Reactions can range from oral itching to systemic anaphylaxis, so awareness is a safety issue.

White rice and baked chicken are not part of the latex-cross-reactive food group and pose no latex-related risk, so they are not correct choices. (Other foods with weaker associations that the client may also be counseled about include tomato, potato, and papaya.)

Beyond diet, latex-allergic clients need a latex-safe care environment: non-latex gloves, latex-free equipment, and clear allergy labeling on the chart and room. A helpful memory aid is that the highest-risk foods — banana, avocado, kiwi, and chestnut — can be recalled as the core of latex-fruit syndrome. Clinical pearl: clients with spina bifida and healthcare workers have elevated rates of latex allergy from repeated exposure, and any latex-allergic client presenting with wheezing, hives, or hypotension after a food or glove exposure should be treated for a possible Type I hypersensitivity reaction, with intramuscular epinephrine first-line if anaphylaxis develops.

Passive immunity is the transfer of preformed antibodies from an outside source, giving immediate but temporary protection because the person's own immune system does not produce them. Receiving rabies immune globulin after an animal bite is a classic example — it delivers ready-made antibodies for instant protection while the separately administered vaccine builds the body's own long-term response. Other examples of passive immunity include maternal antibodies crossing the placenta, antibodies in breast milk, and other immune globulin preparations.

The other options describe active immunity, in which the person's own immune system is stimulated to make antibodies, producing slower-onset but long-lasting protection with memory. The tetanus toxoid vaccine and the hepatitis B vaccine series are examples of artificially acquired active immunity (vaccination), and recovering from chickenpox is naturally acquired active immunity from actual infection.

Clinical pearl: passive = "borrowed" antibodies (immediate, short-lived, no memory), whereas active = "earned" antibodies (delayed onset, durable, with immunologic memory). When a client needs protection right now — after a rabies, tetanus-prone, or hepatitis B exposure — immune globulin provides immediate coverage, and a vaccine is often given at the same time to establish lasting active immunity for the future.