NLE Immune System & Immunologic Disorders — Immunity, Hypersensitivity and Allergic DisordersCheat Sheet
One-page cheat sheet for NLE Immune System & Immunologic Disorders — Immunity, Hypersensitivity and Allergic Disorders. Every formula, definition, and key fact you need for this chapter, condensed to a single printable page. Designed for the final review session before the NLE 2026.
Exam context
For the Philippine Nurse Licensure Examination (PNLE), Professional Regulation Commission (PRC) — Board of Nursing tests Immune System & Immunologic Disorders under a "Core" label, with Immunity, Hypersensitivity and Allergic Disorders in the 1st slot across 2 chapters. NLE candidates must clear the 75% weighted average with no sub-test below 60% cut on the 2026 paper, which draws about 50 Immune System & Immunologic Disorders questions. Date to watch: Bi-annual.
Immunity, Hypersensitivity and Allergic Disorders - Cheat Sheet
Your last-minute revision companion for the immune system chapter. This condensed reference covers immunity types, hypersensitivity reactions, anaphylaxis management, and immunodeficiency — the heaviest-tested topics in the NLE Board of Nursing exam.
Sections
Section Title
Types of Immunity
Important Facts
- Innate immunity is the body's first, rapid, nonspecific defense.
- Adaptive immunity is slower to develop but creates lasting memory via antibodies and sensitized T cells.
- Humoral (B-cell) immunity is antibody-driven; cell-mediated (T-cell) immunity is cytokine and direct cell contact-driven.
- Complement system is part of innate immunity; activated by antibodies (classical) or pathogens (alternative/lectin).
- Phagocytes (neutrophils, macrophages) are key players in both innate and adaptive immunity.
Key Definitions
Term
Innate Immunity
Example
First-line defense against any invader; neutrophil engulfing bacteria.
Definition
Nonspecific, present from birth; immediate response via skin, mucous membranes, phagocytes, inflammation, and complement; no memory.
Term
Adaptive Immunity
Example
Immunity to measles after infection or MMR vaccine; faster response to second exposure.
Definition
Antigen-specific, develops over time with memory; slower first response but faster on re-exposure; mediated by B and T lymphocytes.
Term
Humoral Immunity
Example
IgG and IgM antibodies protecting against bacterial infection.
Definition
B lymphocyte-mediated; produces antibodies (immunoglobulins) against specific antigens.
Term
Cell-Mediated Immunity
Example
T cells destroying virus-infected cells; transplant rejection.
Definition
T lymphocyte-mediated (CD4 helper, CD8 cytotoxic); targets intracellular pathogens and foreign cells.
Diagrams To Know
- Innate vs Adaptive immunity comparison chart
- B cell → plasma cell → antibody production pathway
- T cell development (thymus) and CD4/CD8 distinction
Common Values
Value
21 days (maternal IgG disappears by 6 months in infant if not boosted)
Symbol
t½
Quantity
Serum IgG half-life
Value
5 days
Symbol
t½
Quantity
Serum IgM half-life
Value
6 days
Symbol
t½
Quantity
Serum IgA half-life
Section Title
The Five Immunoglobulins (Antibodies)
Important Facts
- IgG is the ONLY antibody that crosses the placenta — key for passive maternal immunity.
- IgM is FIRST in acute infection; elevated IgM indicates active/recent disease.
- IgA is the second most abundant antibody (after IgG) and protects the gut and respiratory tract.
- IgE is the SMALLEST and LEAST ABUNDANT but the most dangerous — mediates anaphylaxis.
- IgE levels rise in parasitic infections and allergic conditions; measured as total IgE or allergen-specific IgE (RAST).
Key Definitions
Term
IgG
Example
Protects newborn for first 6 months; rises on second exposure to antigen (vaccination booster).
Definition
Most abundant antibody; crosses placenta (passive immunity to newborn); drives secondary immune response; opsonizes pathogens.
Term
IgM
Example
Positive IgM in acute hepatitis or acute strep infection indicates recent/acute disease.
Definition
Largest antibody; first produced in acute/primary infection; does NOT cross placenta; excellent complement activator.
Term
IgA
Example
IgA in breast milk protects infant gut; colostrum is rich in IgA.
Definition
Found in secretions (saliva, tears, breast milk, colostrum, mucous membranes); protects mucosal surfaces; prevents pathogen adhesion.
Term
IgE
Example
IgE crosslinking on mast cell triggers histamine release in anaphylaxis.
Definition
Binds mast cells and basophils; mediates allergic and anaphylactic (Type I) reactions; responsible for immediate hypersensitivity.
Term
IgD
Example
Rarely tested on NLE; remember it is the B cell surface marker.
Definition
Surface receptor on B lymphocytes; role least understood; involved in B cell activation.
Diagrams To Know
- Immunoglobulin structure (Y-shaped, antigen-binding sites, constant and variable regions)
- Antibody distribution in body (serum vs secretions)
- Temporal IgM vs IgG response curve in primary vs secondary infection
Common Values
Value
6 months (can be longer if mother had high IgG titer)
Symbol
t
Quantity
Maternal IgG protection duration in newborn
Value
2–6 weeks (depends on type and dose)
Symbol
t
Quantity
Passive immunoglobulin injection duration
Value
7–14 days post-vaccination
Symbol
t
Quantity
Active vaccine onset (antibody detectable)
Section Title
Types of Acquired Immunity: Active vs Passive
Important Facts
- Active immunity = SLOW onset (days to weeks) but LONG-LASTING (years to life) with MEMORY; body is the factory.
- Passive immunity = IMMEDIATE onset (hours) but TEMPORARY (weeks to months) with NO MEMORY; borrowed antibodies.
- Newborns are protected by maternal IgG (crosses placenta) for ~6 months; after that they are susceptible until vaccinated.
- Breast milk provides IgA (secretory) for mucosal protection; colostrum is especially rich in IgA.
- Live vaccines should NOT be given within 2–3 weeks of passive immunization (antibodies neutralize the vaccine).
- In the Philippines (PRC context), the DOH-recommended vaccination schedule uses active immunization (live attenuated or inactivated vaccines).
Key Definitions
Term
Active Immunity
Example
Vaccination (artificial) or infection (natural); immunity lasts years to lifetime.
Definition
Body makes its own antibodies and sensitized T cells; slow onset, long-lasting with memory.
Term
Passive Immunity
Example
Breast milk IgA (natural) or tetanus immunoglobulin injection (artificial); lasts weeks to months.
Definition
Receives ready-made antibodies from external source; immediate onset, temporary (short-lived) with NO memory.
Term
Natural Active Immunity
Example
Immunity after chickenpox, measles, or COVID-19 infection; lasts years to lifetime.
Definition
Antibodies made AFTER actual infection with the pathogen.
Term
Artificial Active Immunity
Example
MMR vaccine, hepatitis B vaccine, tetanus toxoid; requires booster; lasts 10–15 years typically.
Definition
Antibodies made AFTER vaccination with attenuated or killed antigen (or subunit/toxoid).
Term
Natural Passive Immunity
Example
Newborn protected by maternal IgG for 6 months; breastfed infant receives IgA.
Definition
Ready-made maternal IgG across placenta or IgA/IgG in breast milk; transferred at birth/lactation.
Term
Artificial Passive Immunity
Example
Tetanus immunoglobulin (TIG), hepatitis B immunoglobulin (HBIG), rabies immunoglobulin (RIG); lasts 2–6 weeks.
Definition
Ready-made antibodies given as injection (immune serum, immunoglobulin, antivenom, monoclonal antibody).
Diagrams To Know
- Active vs Passive immunity matrix (natural/artificial × active/passive)
- Timeline: active immunity (slow onset, long duration) vs passive immunity (fast onset, short duration)
- IgG vs IgA levels in breast milk over lactation stages (colostrum → mature milk)
Common Values
Value
Seconds to minutes
Symbol
t
Quantity
Type I onset time
Value
48–72 hours (can read PPD at 48 or 72 hrs)
Symbol
t
Quantity
Type IV reaction peak
Value
≥5 mm (contacts), ≥10 mm (healthcare workers, immunocompetent), ≥15 mm (low risk)
Symbol
d
Quantity
PPD induration threshold for TB exposure
Section Title
The Four Types of Hypersensitivity Reactions (ACID)
Important Facts
- Type I is ANTIBODY-MEDIATED (IgE) and IMMEDIATE (seconds to minutes).
- Type II is ANTIBODY-MEDIATED (IgG/IgM) and results in CELL DESTRUCTION.
- Type III is ANTIBODY-MEDIATED (immune complexes) and results in INFLAMMATION.
- Type IV is NOT ANTIBODY-MEDIATED (T-cell) and is DELAYED (24–72 hours).
- Memory aid: ACID = A (Type I Anaphylactic), C (Type II Cytotoxic), I (Type III Immune complex), D (Type IV Delayed).
- Types I, II, III are antibody-mediated and relatively rapid; Type IV is cell-mediated and slow.
- PPD test is Type IV; induration at 48–72 hours means T-cell sensitization to TB antigen (does NOT prove active TB).
Key Definitions
Term
Type I — Anaphylactic/Allergic
Example
Peanut allergy, bee sting anaphylaxis, latex allergy type I, food allergy.
Definition
IgE-mediated; mast cell and basophil degranulation releasing histamine; immediate (minutes); allergies, anaphylaxis, urticaria, angioedema, asthma.
Term
Type II — Cytotoxic
Example
ABO incompatible transfusion, Rh incompatibility (HDN), autoimmune hemolytic anemia, Graves disease.
Definition
IgG or IgM antibodies against cell surface antigens; complement activation or ADCC; cell destruction; hemolytic reactions.
Term
Type III — Immune Complex
Example
SLE, rheumatoid arthritis, post-streptococcal glomerulonephritis, serum sickness, Arthus reaction.
Definition
Antigen-antibody complexes deposit in tissues; complement activation; inflammation; systemic or local.
Term
Type IV — Delayed/Cell-Mediated
Example
PPD/Mantoux test (tuberculin), contact dermatitis (poison ivy, nickel, latex delayed), transplant rejection, TB granuloma.
Definition
T-cell-mediated (NOT antibody); sensitized T cells release cytokines recruiting macrophages; 24–72 hours onset; granulomatous reactions.
Diagrams To Know
- ACID hypersensitivity classification table (Gell-Coombs)
- Type I pathway: allergen → IgE binding mast cell → degranulation → mediator release → symptoms
- Type IV timeline: antigen → T-cell activation → cytokine release → macrophage recruitment → inflammation (24–72 hrs)
Common Values
Value
≥3 mm above negative control (scratch, prick, or intradermal)
Symbol
d
Quantity
Skin test wheal size indicating sensitization
Value
Minutes to 2 hours (food allergy)
Symbol
t
Quantity
Peak reaction onset after food ingestion
Section Title
Type I Hypersensitivity — Allergic Reactions
Important Facts
- Common allergens: pollen (hay fever), dust mites, mold, animal dander, foods (peanuts, shellfish, eggs, milk), insect venom, medications (penicillin), latex.
- Respiratory manifestations: sneezing, rhinorrhea, nasal congestion, wheezing, cough, dyspnea.
- Skin manifestations: urticaria (hives), pruritus, erythema, angioedema.
- GI manifestations (especially with food allergy): nausea, vomiting, cramping, diarrhea, abdominal pain.
- Ocular manifestations: itching, tearing, conjunctivitis, lacrimation.
- Atopic individuals (family history of allergy, asthma, eczema) are at higher risk for allergies.
- Always ask about drug allergies BEFORE administering any medication — penicillin is the classic drug allergy (IgE-mediated in ~1% of population).
Key Definitions
Term
Allergy
Example
Pollen allergy, dust mite allergy, shellfish allergy, penicillin allergy.
Definition
Type I hypersensitivity to an ordinarily harmless environmental antigen (allergen); IgE-mediated.
Term
Allergen
Example
Pollen, dust mites, peanuts, shellfish, tree nuts, eggs, milk, latex, penicillin.
Definition
Environmental or dietary substance that triggers IgE production and allergic reaction in susceptible individuals.
Term
Sensitization
Example
First bee sting — person develops IgE but does not react; second sting triggers anaphylaxis.
Definition
First exposure to allergen; IgE antibodies are produced and bind to mast cells; no symptoms yet.
Term
Urticaria
Example
Food or drug allergy presenting with itchy wheals; usually transient.
Definition
Hives; raised, itchy wheals on skin from mast cell degranulation and histamine release.
Term
Angioedema
Example
Angioedema of tongue/pharynx in severe allergic reaction or ACE-inhibitor side effect.
Definition
Deep tissue swelling (dermis and submucosa) of lips, tongue, face, eyelids from increased capillary permeability; can obstruct airway.
Diagrams To Know
- Allergy diagnostic algorithm (history → skin test/RAST → management)
- Mast cell degranulation pathway (allergen + IgE → crosslinking → calcium influx → mediator release)
- Spectrum of allergic reactions (rhinitis → urticaria → angioedema → bronchospasm → anaphylaxis)
Common Values
Value
<100 IU/mL (varies by lab)
Symbol
IgE
Quantity
Normal serum IgE
Value
50–500/μL
Symbol
Eos
Quantity
Normal eosinophil count
Section Title
Allergy Diagnostics
Important Facts
- Skin testing is rapid, inexpensive, and specific; requires patient off antihistamines for 3–5 days and emergency equipment at hand.
- RAST/ImmunoCAP is useful when skin testing is contraindicated (severe dermatitis, patient on antihistamines, risk of anaphylaxis).
- Wheal size correlates with degree of sensitization but not necessarily severity of clinical reaction.
- Negative skin test does NOT completely rule out allergy; clinical correlation is essential.
- Eosinophilia is present in allergy, asthma, and parasitic infections but is nonspecific.
Key Definitions
Term
Skin Testing (Prick/Scratch/Intradermal)
Example
Patient with allergic rhinitis tested with pollen extract; ≥3 mm wheal at 15–20 minutes = positive.
Definition
Allergen introduced into epidermis; wheal-and-flare reaction indicates IgE sensitization; must have emergency equipment available.
Term
RAST (Radioallergosorbent Test) / ImmunoCAP
Example
Positive RAST for peanut IgE confirms IgE-mediated peanut allergy.
Definition
Serum test measuring allergen-specific IgE antibody; in vitro; safer than skin testing; useful if patient on antihistamines or has severe dermatitis.
Term
Total Serum IgE
Example
Elevated total IgE in allergic rhinitis or atopic asthma; also elevated in hookworm or ascaris.
Definition
Measures all circulating IgE; elevated in allergy and parasitic infections; nonspecific.
Term
Eosinophilia
Example
CBC shows eosinophilia in allergic asthma, eczema, or roundworm infection.
Definition
Elevated eosinophil count (>500/μL); supports allergic or parasitic process; nonspecific.
Diagrams To Know
- Allergy diagnostic flowchart (history → skin test or RAST → positive → avoidance/treatment)
- Wheal-and-flare reaction interpretation (at 15–20 minutes post-prick)
Common Values
Value
1–3 hours
Symbol
t
Quantity
Onset of second-generation antihistamine effect
Value
12–24 hours (depends on agent)
Symbol
t
Quantity
Duration of antihistamine effect
Section Title
Allergy Pharmacology
Important Facts
- First-generation antihistamines (diphenhydramine, chlorpheniramine) are lipid-soluble, cross BBB, cause drowsiness, anticholinergic effects; avoid in drivers.
- Second-generation antihistamines (cetirizine, loratadine, fexofenadine) are more selective, less sedating, safer in elderly.
- Corticosteroids reduce inflammation but are NOT first-line for acute allergic reactions (that is epinephrine for anaphylaxis); used for prophylaxis and chronic allergy.
- Never stop systemic corticosteroids abruptly — taper to avoid adrenal crisis.
- Mast cell stabilizers and leukotriene modifiers are prophylactic; not for acute relief.
- Decongestants are sympathomimetics; contraindicated in uncontrolled hypertension, coronary artery disease, hyperthyroidism.
- Epinephrine (NOT antihistamines or steroids) is the ONLY first-line emergency drug for anaphylaxis.
Key Definitions
Term
Antihistamines (H1-receptor blockers)
Example
Diphenhydramine (sedating), cetirizine, loratadine, fexofenadine (non-sedating); avoid diphenhydramine in drivers or elderly.
Definition
Block histamine at H1 receptors; first-generation (sedating) vs second-generation (non-sedating); manage urticaria, rhinitis, conjunctivitis.
Term
Corticosteroids
Example
Intranasal fluticasone for allergic rhinitis; prednisone for severe allergic reaction; DO NOT stop abruptly.
Definition
Reduce inflammation; systemic (prednisone) or topical (nasal spray, inhaler); for moderate-severe or chronic allergy.
Term
Mast Cell Stabilizers
Example
Cromolyn nasal spray 2–4 times daily before allergen exposure to prevent rhinitis.
Definition
Prevent mast cell degranulation; cromolyn sodium; prophylactic use; slower onset than antihistamines.
Term
Leukotriene Modifiers
Example
Montelukast 10 mg daily at bedtime for persistent allergic asthma.
Definition
Block leukotriene receptors or synthesis; montelukast, zafirlukast; useful for allergic asthma and rhinitis.
Term
Decongestants
Example
Pseudoephedrine for nasal congestion; AVOID if BP >180 mmHg or on MAOI.
Definition
α-adrenergic agonists (pseudoephedrine, phenylephrine); relieve nasal congestion; avoid in hypertension.
Term
Immunotherapy (Allergen Desensitization)
Example
Pollen immunotherapy for seasonal allergic rhinitis; requires months to years and ongoing maintenance.
Definition
Gradual exposure to increasing allergen doses subcutaneously or sublingually; induces immune tolerance; slow but potentially curative.
Diagrams To Know
- Antihistamine classification (H1 vs H2; first-gen vs second-gen; pharmacokinetics)
- Allergy medication algorithm (mild → antihistamine; moderate → add intranasal steroid; severe → add leukotriene modifier or consider immunotherapy)
Formulas
Formula
Epinephrine dose (adult) = 0.3–0.5 mg of 1:1000 (1 mg/mL) IM
Meaning
Adult dose for anaphylaxis; 1:1000 is the CONCENTRATION (not dilution ratio); IM is the ROUTE (anterolateral thigh/vastus lateralis); repeat every 5–15 min as needed.
Watch Out
COMMON MISTAKE: confusing 1:1000 (IM for anaphylaxis) with 1:10,000 (IV for cardiac arrest). NEVER give 1:1000 IV — it is too concentrated and will cause severe hypertension/arrhythmia. The 1:1000 IM in the thigh is absorbed more slowly and is safer. Also WRONG: waiting for airway obstruction — treat at FIRST signs (throat tightness, hoarseness, urticaria with respiratory signs).
When To Use
First sign of anaphylaxis (airway symptoms, hypotension, severe bronchospasm, angioedema, shock). ADMINISTER IMMEDIATELY — no delay for IV access or testing.
Formula
Epinephrine dose (pediatric) = 0.01 mg/kg IM (1:1000), max 0.3 mg
Meaning
Pediatric dose based on weight; same concentration (1:1000) and route (IM); capped at 0.3 mg to match the smallest typical adult dose.
Watch Out
COMMON MISTAKE: using body surface area or dose based on adult formulas without weight conversion. Use 0.01 mg/kg precisely. For a 30 kg child: 0.01 × 30 = 0.3 mg IM.
When To Use
Child with anaphylaxis; calculate dose as 0.01 × (weight in kg), up to 0.3 mg.
Common Values
Value
Seconds to minutes (typically <10 minutes)
Symbol
t
Quantity
Onset of anaphylaxis symptoms
Value
5–30 minutes
Symbol
t
Quantity
Peak anaphylaxis symptoms
Value
IMMEDIATELY (within seconds); every 5–15 minutes if recurrent symptoms
Symbol
t
Quantity
Time window for epinephrine administration
Value
Minimum 4–8 hours (longer if severe or biphasic)
Symbol
t
Quantity
Observation period post-anaphylaxis
Value
12–18 months (marked on device); check expiry regularly
Symbol
t
Quantity
Epinephrine auto-injector shelf life
Section Title
Anaphylaxis — Life-Threatening Emergency
Important Facts
- ANAPHYLAXIS IS A MEDICAL EMERGENCY — epinephrine must be given IM within SECONDS of onset; delaying for IV access or other interventions risks death.
- Epinephrine ADULT dose: 0.3–0.5 mg of 1:1000 IM (anterolateral thigh); PEDIATRIC: 0.01 mg/kg IM (max 0.3 mg). Repeat every 5–15 minutes as needed.
- Epinephrine 1:1000 is given IM (NOT IV) for anaphylaxis. Epinephrine 1:10,000 is for IV use in cardiac arrest ONLY. Confusing these is FATAL.
- Onset of anaphylaxis is SECONDS to MINUTES after exposure; angioedema, urticaria, and respiratory symptoms are early signs.
- Airway obstruction from laryngeal edema is the LEADING CAUSE OF DEATH in anaphylaxis.
- Administer high-flow oxygen and prepare for intubation or emergency cricothyrotomy if stridor or inability to swallow develops.
- Establish IV access and give rapid isotonic crystalloid (normal saline, LR) for hypotension; vasopressors (norepinephrine) may be needed if shock persists.
- Antihistamines (diphenhydramine) and H2-blockers (ranitidine/famotidine) are ADJUNCTS; they are FAR TOO SLOW for first-line (take 30 min to hours).
- Corticosteroids (hydrocortisone, methylprednisolone) help prevent BIPHASIC REACTION; give IM or IV after epinephrine.
- Bronchodilators (nebulized salbutamol) for persistent bronchospasm; not a substitute for epinephrine.
- ALL patients must be observed for AT LEAST 4–8 hours (or longer if severe) for biphasic reaction; do NOT discharge immediately.
- Patients with anaphylaxis should be prescribed an epinephrine auto-injector to carry at ALL times (EpiPen, EpiPen Jr); teach self-administration into outer thigh through clothing if needed.
- Common triggers in the Philippines: peanuts, shellfish (especially in coastal areas), medications (penicillin), insect venom (wasps, fire ants), latex gloves in healthcare.
Key Definitions
Term
Anaphylaxis
Example
Anaphylaxis to peanut, bee sting, penicillin injection, latex glove, IV contrast medium.
Definition
Severe, rapid, systemic type I hypersensitivity reaction; massive mediator release causing distributive shock, airway edema, and bronchospasm; life-threatening within minutes.
Term
Biphasic Anaphylaxis
Example
Patient treated for anaphylaxis, improves, then deteriorates 4 hours later; 5–15% of severe anaphylaxis cases.
Definition
Initial anaphylaxis followed by recurrence of symptoms hours (1–72 hours) later without re-exposure; due to late-phase mediator release.
Term
Laryngeal Edema
Example
Patient with anaphylaxis develops stridor and inability to swallow; imminent airway compromise.
Definition
Swelling of larynx from increased capillary permeability; may cause stridor, hoarseness, throat tightness, complete airway obstruction.
Diagrams To Know
- Anaphylaxis management algorithm (recognize → epinephrine 0.3–0.5 mg IM → airway → oxygen → IV access → fluids → antihistamine → steroid → observe 4–8 hours for biphasic reaction)
- Epinephrine auto-injector landmarks (anterolateral thigh/vastus lateralis is the correct injection site)
- Anaphylaxis timeline (onset seconds to minutes, peak at 5–30 minutes, biphasic peak at 1–72 hours)
Reactions Or Equations
Note
Histamine is rapid-acting (vasodilation, ↑ permeability, bronchospasm); leukotrienes contribute to prolonged bronchospasm and are slower to develop; this is why biphasic reactions occur.
Equation
Anaphylaxis pathophysiology: Allergen + IgE on mast cell/basophil → Crosslinking → Ca2+ influx → Degranulation → Histamine, tryptase, leukotrienes, prostaglandins → Vasodilation, ↑ capillary permeability, bronchoconstriction, smooth muscle contraction → Shock, airway edema, bronchospasm
Conditions
Type I hypersensitivity; occurs on re-exposure after sensitization; mediated by preformed (histamine) and newly synthesized (leukotrienes, prostaglandins) mediators.
Section Title
Latex Allergy
Important Facts
- Latex allergy prevalence is ~1–3% in general population; much higher in healthcare workers (~10%) and individuals with spina bifida (25–60%).
- HIGH-RISK GROUPS: healthcare workers (glove exposure), patients with spina bifida (repeated catheterizations and medical procedures), patients with history of multiple surgeries (latex equipment exposure).
- Type IV latex allergy is more common (delayed dermatitis from accelerators) but Type I (IgE-mediated) is more dangerous (anaphylaxis).
- Latex-fruit cross-reactivity: banana, avocado, kiwi, chestnut; hickory nuts and sweet potato also reported; avoidance is important for latex-allergic patients.
- LATEX-CONTAINING ITEMS IN HEALTHCARE: gloves, catheters, endotracheal tubes, chest tubes, blood pressure cuff tubing, stethoscope diaphragms, elastic in drapes.
- LATEX-FREE ALTERNATIVES: nitrile gloves, vinyl gloves (less reliable), synthetic catheters, silicone tubes, cloth BP cuff.
Key Definitions
Term
Latex Allergy — Type IV (Delayed Contact Dermatitis)
Example
Healthcare worker develops eczema on hands after latex glove use; worsens over days; resolves after glove removal.
Definition
Most common form; eczematous reaction to latex proteins or accelerators (e.g., thiuram derivatives); onset 24–48 hours; localized to contact area.
Term
Latex Allergy — Type I (Immediate IgE)
Example
Anaphylaxis during surgical procedure from latex glove contact; requires immediate epinephrine.
Definition
Less common but dangerous; IgE-mediated immediate reaction; urticaria, angioedema, bronchospasm, anaphylaxis; life-threatening.
Term
Latex-Fruit Cross-Reactivity
Example
Patient with latex allergy develops oral itching/angioedema after eating banana (cross-reactive protein).
Definition
IgE antibodies to latex cross-react with proteins in certain fruits; patient allergic to latex may react to banana, avocado, kiwi, chestnut.
Diagrams To Know
- Latex allergy types (Type IV contact dermatitis vs Type I anaphylaxis)
- Latex-fruit cross-reactivity tree (latex → banana, avocado, kiwi, chestnut)
- Latex-free healthcare setup (gloves, equipment, environment)
Section Title
Nursing Management of Latex Allergy
Important Facts
- IDENTIFY latex-allergic patients on admission; document prominently in chart and use alert stickers/flags.
- CREATE A LATEX-FREE ENVIRONMENT: stock unit with non-latex gloves (nitrile), use latex-free equipment (catheters, endotracheal tubes, BP cuff).
- SCHEDULE latex-sensitive patients as FIRST SURGICAL CASE OF THE DAY to minimize airborne latex powder in the OR (latex particles can float in air for hours).
- EDUCATE patient: avoid latex gloves, balloons, condoms, rubber bands; use non-latex condoms (polyurethane, lambskin); inform all healthcare providers.
- KEEP EMERGENCY EQUIPMENT AT BEDSIDE: epinephrine auto-injector, oxygen, emergency medications for Type I anaphylaxis.
- EDUCATE about latex-fruit cross-reactivity: avoid or be cautious with banana, avocado, kiwi, chestnut.
- For Type IV contact dermatitis: recommend emollients, low-potency topical corticosteroids, and strict latex avoidance.
Key Definitions
Term
Latex-Free Environment
Example
OR prep for spina bifida patient includes nitrile gloves, latex-free catheters, synthetic equipment; first case of the day to minimize airborne latex.
Definition
Healthcare setting using non-latex gloves, equipment, and supplies for a latex-allergic patient; requires advance identification and preparation.
Diagrams To Know
- Pre-surgical checklist for latex-allergic patient (identify → stock latex-free → schedule first → communicate to OR team)
Common Values
Value
500–1500 cells/μL
Symbol
CD4
Quantity
Normal CD4 T-cell count
Value
<200 cells/μL
Symbol
CD4
Quantity
CD4 count defining AIDS
Value
<200 cells/μL
Symbol
CD4
Quantity
CD4 threshold for PCP prophylaxis (TMP-SMX)
Value
<50 cells/μL
Symbol
CD4
Quantity
CD4 threshold for MAC prophylaxis (azithromycin)
Value
2000–7500/μL (or ANC >1500/μL)
Symbol
ANC
Quantity
Normal neutrophil count
Value
ANC <1500/μL
Symbol
ANC
Quantity
Neutropenia threshold
Value
ANC <500/μL
Symbol
ANC
Quantity
Severe neutropenia
Value
70–400 mg/dL
Symbol
IgA
Quantity
Normal serum IgA
Section Title
Immunodeficiency — Primary and Secondary
Important Facts
- PRIMARY immunodeficiency is rare; SECONDARY immunodeficiency (HIV/AIDS, chemo, steroids) is common in clinical practice.
- SCID is the classic primary immunodeficiency affecting BOTH B and T cells; historically called 'bubble boy disease'; now treatable with stem cell transplant or gene therapy.
- Selective IgA deficiency is the MOST COMMON primary immunodeficiency in Caucasians (~1 in 300) but often asymptomatic; risk of transfusion reaction if given IgA-containing blood.
- DiGeorge syndrome (22q11 deletion) involves thymic hypoplasia, T-cell deficiency, cardiac defects, cleft palate, hypocalcemia; variable severity from mild to severe SCID-like.
- Bruton agammaglobulinemia (X-linked) is B-cell deficiency; presents with severe bacterial infections after maternal IgG wanes at 6 months.
- HIV/AIDS: CD4 count <200 defines AIDS; increased risk of PCP, toxoplasmosis, CMV, TB, MAC, oropharyngeal candidiasis; requires ART and prophylaxis (TMP-SMX, azithromycin).
- Neutropenia (<1500 ANC) increases infection risk; severe neutropenia (<500) requires protective/neutropenic precautions; fever is treated as INFECTION UNTIL PROVEN OTHERWISE.
- Causes of secondary immunodeficiency: HIV/AIDS, cancer (leukemia, lymphoma), chemotherapy, radiation, corticosteroids, immunosuppressants, malnutrition, splenectomy, aging.
- In the Philippines, HIV/AIDS and TB are significant secondary immunodeficiencies; DOH guidelines recommend ART initiation regardless of CD4 count (same-day initiation in some cases).
Key Definitions
Term
Primary (Congenital) Immunodeficiency
Example
Severe combined immunodeficiency (SCID); defects in both B and T cells; presents with recurrent infections in infancy.
Definition
Inherited genetic defect present from birth; affects B cells, T cells, or both; rare but severe; examples: SCID, DiGeorge, Bruton agammaglobulinemia.
Term
Secondary (Acquired) Immunodeficiency
Example
HIV/AIDS with CD4 <200; increased risk of PCP, toxoplasmosis, TB, OI; chemotherapy causing neutropenia.
Definition
Results from another disease, treatment, or condition; far more common than primary; examples: HIV/AIDS, malignancy, chemotherapy, steroids.
Term
Severe Combined Immunodeficiency (SCID)
Example
SCID infant isolated in 'bubble' to prevent infection; requires hematopoietic stem cell transplant or gene therapy.
Definition
Defects in both B and T lymphocytes; autosomal recessive or X-linked; presents in infancy with severe infections, failure to thrive, death without treatment.
Term
DiGeorge Syndrome
Example
Infant with cleft palate, congenital heart disease, hypoparathyroidism, and T-cell deficiency.
Definition
22q11 deletion; thymic aplasia/hypoplasia; T-cell deficiency; cardiac, facial, cleft palate abnormalities; variable severity.
Term
HIV/AIDS
Example
Patient with CD4 <200 at high risk for PCP, CMV, toxoplasmosis, TB, MAC; requires antiretroviral therapy (ART) and prophylaxis.
Definition
Virus destroying CD4 T cells; progressive immunodeficiency; AIDS defined as CD4 <200 cells/μL or presence of AIDS-defining opportunistic infection.
Term
Neutropenia
Example
Chemotherapy-induced neutropenia; patient isolated with protective precautions; fever is treated as infection until proven otherwise.
Definition
Absolute neutrophil count (ANC) <1500/μL; increased infection risk; severe neutropenia <500 ANC.
Diagrams To Know
- Primary vs Secondary immunodeficiency classification tree
- CD4 count and opportunistic infection risk in HIV/AIDS (CD4 >200, 100–200, <100)
- Neutropenia severity classification (mild 1000–1500, moderate 500–1000, severe <500)
Section Title
Nursing Management of Immunodeficiency
Important Facts
- HAND HYGIENE is the SINGLE MOST IMPORTANT infection-prevention measure; educate patient and visitors.
- PRIVATE ROOM for severely immunocompromised patients (CD4 <50, ANC <500); HIGH-EFFICIENCY PARTICULATE AIR (HEPA) filtration may be used.
- AVOID CROWDS and instruct patient to avoid public places during high-risk periods (flu season, measles outbreaks).
- STRICT ASEPSIS for all invasive procedures; use closed IV infusion systems; change dressings with aseptic technique.
- NO FRESH FLOWERS, PLANTS, or STANDING WATER (aspergillus and other fungal sources).
- NO RAW FRUITS, VEGETABLES, or UNPASTEURIZED DAIRY; recommend cooked/processed foods to reduce bacterial contamination.
- LIVE VACCINES ARE CONTRAINDICATED in significant immunodeficiency (CD4 <200, ANC <500); inactivated vaccines may be given but response may be poor.
- MONITOR FOR FEVER and subtle signs of infection (cough, dyspnea, dysuria, diarrhea, perirectal pain); REPORT IMMEDIATELY; fever is treated as INFECTION UNTIL PROVEN OTHERWISE.
- For severe neutropenia, empiric broad-spectrum antibiotics (after blood cultures) are initiated even if source is unknown.
- IVIG infusion: start slowly (0.5 mL/kg/hr), titrate up to 4 mL/kg/hr; monitor for headache, chest pain, hypotension, anaphylaxis; pre-medicate with acetaminophen/diphenhydramine.
- EDUCATE patient: importance of ART compliance in HIV; when to seek care; signs of OI; prevent TB/MAC with prophylaxis; nutrition and rest; smoking cessation.
Key Definitions
Term
Protective (Neutropenic) Precautions
Example
Chemotherapy patient with ANC <500 in private room with NO VISITORS with respiratory illness; hand hygiene before and after care.
Definition
Infection-prevention measures for immunocompromised patient: meticulous hand hygiene, private room, avoid crowds, screen for infection, strict asepsis, no fresh flowers/raw fruits.
Term
Intravenous Immunoglobulin (IVIG)
Example
Patient with Bruton agammaglobulinemia receives IVIG every 3–4 weeks to replace IgG; infuse slowly to avoid volume overload and anaphylaxis.
Definition
Pooled antibodies from donor plasma; used for antibody deficiencies; given IV slowly over 2–6 hours; monitor for adverse reactions.
Diagrams To Know
- Protective precautions checklist (hand hygiene → private room → visitors screened → no flowers/raw foods → aseptic technique → fever alert)
- Opportunistic infection prevention by CD4 count (CD4 <200 → TMP-SMX; CD4 <100 → add antifungal; CD4 <50 → add MAC prophylaxis)
Common Values
Value
0.3 mL fetal RBCs (can detect by Kleihauer-Betke or flow cytometry)
Symbol
V
Quantity
Minimal incompatible RBC volume for sensitization
Value
300 μg IM at 28 weeks and within 72 hours of delivery (or 100 μg per mL fetal RBCs transfused)
Symbol
d
Quantity
Standard RhoGAM dose
Section Title
Type II Hypersensitivity — Cytotoxic Reactions (Quick Reference)
Important Facts
- Type II reactions are mediated by IgG and IgM against cell surface antigens; lead to cell destruction via complement (C3b opsonization, MAC) or ADCC (antibody-dependent cellular cytotoxicity).
- ABO TRANSFUSION REACTIONS: ABO antibodies (IgM) are naturally occurring; reactions are severe and IMMEDIATE (minutes); incompatibility is FATAL if not stopped immediately.
- Rh INCOMPATIBILITY: First Rh+ pregnancy in Rh- mother usually asymptomatic (IgM antibodies, do not cross placenta well); second Rh+ pregnancy at risk of HDN (IgG crosses placenta).
- RhoGAM (Rh immunoglobulin) is given to Rh- mother at 28 weeks gestation and within 72 hours of delivery of Rh+ baby; prevents Rh sensitization in future pregnancies.
- Graves disease (Type II): IgG anti-TSH receptor antibodies stimulate thyroid → hyperthyroidism (unique in that it is stimulating, not destructive).
- Myasthenia gravis: IgG anti-acetylcholine receptor antibodies → blockade and destruction of NMJ → muscle weakness.
- Goodpasture syndrome: IgG anti-glomerular basement membrane (GBM) → glomerulonephritis and pulmonary hemorrhage.
- Autoimmune hemolytic anemia: IgG anti-RBC surface antigens → RBC destruction (extravascular by spleen, sometimes intravascular).
Key Definitions
Term
Type II Hypersensitivity
Example
ABO incompatible transfusion, Rh incompatibility (hemolytic disease of newborn), autoimmune hemolytic anemia.
Definition
IgG or IgM antibodies bind cell surface antigens; complement activation or ADCC; cell destruction; hemolytic or cytotoxic.
Term
ABO Incompatible Transfusion (Acute Hemolytic)
Example
Type A patient transfused with type B blood; severe hemolysis, hemoglobinuria, hypotension, renal failure, DIC, death if severe.
Definition
Recipient has IgM antibodies to donor RBC antigens (anti-A or anti-B); immediate complement activation and intravascular hemolysis.
Term
Rh Incompatibility (Hemolytic Disease of Newborn, HDN)
Example
Rh-negative mother with Rh-positive fetus; first pregnancy usually mild; second Rh+ pregnancy at risk of severe HDN; prevented by RhoGAM.
Definition
Rh-negative mother sensitized by Rh-positive fetal blood (during pregnancy or at delivery); IgG crosses placenta in subsequent pregnancy; hemolysis of fetal RBCs.
Diagrams To Know
- ABO transfusion compatibility matrix (Type A, B, AB, O donors and recipients)
- Rh sensitization pathway in pregnancy (sensitization in first pregnancy → antibody production → HDN in subsequent pregnancy → RhoGAM prevention)
Common Values
Value
7–14 days after exposure (sometimes as late as 3 weeks)
Symbol
t
Quantity
Onset of serum sickness
Section Title
Type III Hypersensitivity — Immune Complex Reactions (Quick Reference)
Important Facts
- Type III involves immune complex deposition and COMPLEMENT ACTIVATION → inflammation → tissue damage.
- Complexes form in ANTIGEN EXCESS (too much antigen, not enough antibody) because they are too large to be cleared and precipitate in tissues.
- SLE: anti-nuclear antibodies (ANA), anti-dsDNA, anti-histone → immune complexes in kidneys (lupus nephritis), joints, skin → glomerulonephritis, arthritis, rash.
- Post-streptococcal glomerulonephritis: follows Group A Strep infection (pharyngitis/impetigo); immune complexes deposit in glomeruli → hematuria, proteinuria, reduced GFR.
- SERUM SICKNESS: reaction to foreign protein (horse antivenom, antiserum, monoclonal antibodies) or certain drugs (amoxicillin, sulfonamides); onset 7–14 days; self-limited.
- Serum sickness manifestations: FEVER, RASH (urticarial, maculopapular), ARTHRALGIA/ARTHRITIS (especially knees, ankles, wrists), LYMPHADENOPATHY; rare: glomerulonephritis, vasculitis.
- Treatment of serum sickness: antihistamines, NSAIDs, systemic corticosteroids (prednisone) if moderate-severe; self-limited, resolves in weeks.
Key Definitions
Term
Type III Hypersensitivity
Example
SLE, rheumatoid arthritis, post-streptococcal glomerulonephritis, serum sickness, Arthus reaction.
Definition
Antigen-antibody complexes deposit in tissues (joints, skin, blood vessels, kidneys); complement activation; inflammation.
Term
Serum Sickness
Example
Patient given horse tetanus antitoxin develops fever, urticarial rash, joint pain 7–14 days later.
Definition
Type III reaction to foreign serum (e.g., horse antivenom, monoclonal antibodies) or medications (β-lactams); immune complexes deposit → fever, rash, arthritis, lymphadenopathy.
Term
Arthus Reaction
Example
Intradermal antigen injection in pre-sensitized person; local tissue necrosis at injection site.
Definition
Local Type III reaction; antigen-antibody complex deposits in skin; erythema, edema, necrosis within hours.
Diagrams To Know
- Immune complex formation and deposition (antigen in excess → complex formation → vascular/tissue deposition → complement activation → inflammation)
Section Title
Quick Summary Table: Hypersensitivity Types
Diagrams To Know
- See comparison_tables section for detailed hypersensitivity comparison
Must Remember
Item
ANAPHYLAXIS FIRST-LINE DRUG: Epinephrine 0.3–0.5 mg IM (1:1000, 1 mg/mL concentration) into ANTEROLATERAL THIGH (vastus lateralis), repeat every 5–15 min. PEDIATRIC: 0.01 mg/kg IM (max 0.3 mg). DO NOT DELAY for IV access. NEVER give 1:1000 IV (too concentrated, causes severe hypertension); 1:10,000 IV is for cardiac arrest ONLY.
Rank
1
Item
IgE mediates Type I (allergic/anaphylactic) hypersensitivity via mast cell and basophil degranulation. IgG crosses the placenta (only Ig to do so) and provides passive immunity to newborn for ~6 months. IgM is FIRST in acute infection (elevations indicate recent/acute disease). IgA is in secretions and protects mucosal surfaces; colostrum is IgA-rich.
Rank
2
Item
The FOUR HYPERSENSITIVITY TYPES (ACID): I = Anaphylactic (IgE, mast cell, immediate, seconds-min); II = Cytotoxic (IgG/IgM, complement, cell destruction, ABO transfusion); III = Immune Complex (Ag-Ab complexes, complement, SLE/serum sickness); IV = Delayed (T-cell, 24–72 hrs, PPD test, contact dermatitis). Types I–III are antibody-mediated; IV is NOT.
Rank
3
Item
Active immunity (infection or vaccine) is SLOW onset (days to weeks) but LONG-LASTING (years to life) with MEMORY. Passive immunity (placenta, breast milk, Ig injection) is IMMEDIATE onset but TEMPORARY (weeks to months) with NO memory. Newborn is protected by maternal IgG for ~6 months.
Rank
4
Item
AIRWAY OBSTRUCTION from laryngeal edema is the LEADING CAUSE OF DEATH in anaphylaxis. Administer high-flow oxygen immediately; prepare for intubation or emergency cricothyrotomy if stridor or inability to swallow develops. Do NOT wait for complete airway obstruction.
Rank
5
Item
LATEX ALLERGY: High risk in healthcare workers, spina bifida patients, and those with multiple surgeries. Type I (immediate IgE, can cause anaphylaxis) and Type IV (delayed contact dermatitis). Cross-reacts with banana, avocado, kiwi, chestnut. Schedule latex-allergic patients as FIRST CASE OF THE DAY in OR to minimize airborne latex.
Rank
6
Item
BIPHASIC ANAPHYLAXIS: Initial reaction improves, then recurs 1–72 hours later without re-exposure; occurs in ~5–15% of severe anaphylaxis. Reason: late-phase mediator release. All anaphylaxis patients require MINIMUM 4–8 hours observation (longer if severe). Give corticosteroids to prevent biphasic reaction.
Rank
7
Item
ANTIHISTAMINES and CORTICOSTEROIDS are ADJUNCTS in anaphylaxis, NOT first-line. They are far too slow (30 min to hours). Antihistamines do NOT open airways or raise BP. Epinephrine ALONE does both instantly. Always give epinephrine FIRST, then add antihistamines and steroids.
Rank
8
Item
PRIMARY IMMUNODEFICIENCY (rare, congenital): SCID (both B and T cells, fatal without transplant), DiGeorge (T-cell/thymic defect), Bruton agammaglobulinemia (B-cell deficiency). SECONDARY IMMUNODEFICIENCY (common, acquired): HIV/AIDS (CD4 <200 = AIDS), cancer, chemotherapy, steroids, malnutrition. LIVE VACCINES contraindicated in significant immunodeficiency.
Rank
9
Item
In immunodeficiency: Use PROTECTIVE/NEUTROPENIC PRECAUTIONS (hand hygiene, private room, no crowds, no fresh flowers/raw food). Monitor for FEVER as sign of INFECTION (treat fever as infection UNTIL PROVEN OTHERWISE). CD4 <200 in HIV → PCP prophylaxis (TMP-SMX); CD4 <50 → MAC prophylaxis (azithromycin). Educate on ART compliance, safe sex, symptom reporting.
Rank
10
Last Minute Tips
Tip
In anaphylaxis scenarios, ALWAYS choose EPINEPHRINE 0.3–0.5 mg IM as the FIRST action — not antihistamines, not IV access, not positioning (though these follow). If the question says 'patient with stridor and hypotension after peanut ingestion,' the answer is epinephrine IM NOW, THEN airway support. This is the most heavily tested single intervention in the NLE nursing portion.
Tip Number
1
Tip
Memorize the ACID mnemonic for hypersensitivity types and the TIMING: Type I = seconds to minutes (IMMEDIATE); Types II/III = minutes to hours (RAPID); Type IV = 24–72 hours (DELAYED). Test questions often ask 'which type occurs in hours?' and the trap is Type I (it is seconds-minutes, NOT hours). Type IV is always the slow one.
Tip Number
2
Tip
In any immunodeficiency scenario, FEVER = INFECTION UNTIL PROVEN OTHERWISE. Do NOT wait for culture results. In HIV patients with CD4 <200, 'fever + headache' likely means meningitis/meningococcemia/TB; 'fever + cough' likely means PCP. Know the prophylaxis thresholds: TMP-SMX for CD4 <200; MAC prophylaxis for CD4 <50.
Tip Number
3
Tip
PPD (tuberculin/Mantoux) test is Type IV hypersensitivity — READ AT 48–72 HOURS, MEASURE INDURATION (NOT erythema). A positive test means T-cell sensitization to TB antigen (past or current infection), NOT necessarily active TB disease. Requires further workup (CXR, symptoms, culture) to confirm active TB.
Tip Number
4
Tip
If a question mentions LATEX ALLERGY and OR setting: immediately think 'NITRILE GLOVES, LATEX-FREE EQUIPMENT, FIRST CASE OF THE DAY, epinephrine at bedside.' If cross-reactivity is mentioned, the typical fruits are BANANA, AVOCADO, KIWI, CHESTNUT (mnemonic: BACK = Banana, Avocado, Chestnut, Kiwi). Do not confuse latex Type I (anaphylaxis) with Type IV (contact dermatitis hours later).
Tip Number
5
Comparison Tables
Rows
Values
- IgE
- Mast cell/basophil degranulation (histamine, tryptase, leukotrienes)
- Minutes
- Anaphylaxis, urticaria, angioedema, allergic rhinitis, food/drug allergy, asthma, latex allergy type I
- Immediate; biphasic possible; epinephrine IM is first-line; can be life-threatening
Property
Type I (Anaphylactic/Allergic)
Values
- IgG, IgM
- Complement activation or ADCC; cell surface antigen targeted
- Minutes to hours
- ABO transfusion reaction, Rh incompatibility (HDN), autoimmune hemolytic anemia, Graves disease, myasthenia gravis, Goodpasture
- Cell destruction; hemolysis possible; may be intravascular or extravascular
Property
Type II (Cytotoxic)
Values
- IgG, IgM (in complexes)
- Immune complex deposition; complement activation; inflammation
- Hours to days
- SLE, rheumatoid arthritis, post-strep glomerulonephritis, serum sickness, Arthus reaction
- Complexes deposit in tissues/vessels; vasculitis, glomerulonephritis, arthritis; self-limited in serum sickness
Property
Type III (Immune Complex)
Values
- None (T-cell mediated)
- Sensitized T cells release cytokines; macrophage recruitment; granulomatous inflammation
- 24–72 hours
- Tuberculin (PPD) test, contact dermatitis (latex, poison ivy, nickel), transplant rejection, TB granuloma, graft-versus-host disease
- NOT antibody-mediated; local or systemic; induration at 48–72 hrs; can be chronic (TB)
Property
Type IV (Delayed/Cell-Mediated)
Columns
- Type
- Antibody/Mediator
- Mechanism
- Onset
- Examples
- Key Features
Table Title
Four Types of Hypersensitivity Reactions (Gell-Coombs)
Rows
Values
- Most abundant (~70–80% serum Ig)
- 150 kDa
- YES (only Ig to cross)
- NO (IgM is first)
- Serum, tissue fluid, CSF
- Secondary response, opsonization, complement activation, maternal immunity to newborn
- 21 days
Property
IgG
Values
- ~10% serum Ig
- 900 kDa (largest)
- NO
- YES (first in primary infection)
- Serum, lymphoid tissue
- Primary immune response, excellent complement activator, cannot cross placenta
- 5 days
Property
IgM
Values
- Second most abundant (~15–20%)
- 160 kDa (dimer in secretions)
- NO (but secreted in breast milk/colostrum)
- NO
- Secretions (saliva, tears, milk, respiratory/GI mucosa)
- Mucosal immunity, prevents pathogen adhesion, found in colostrum (IgA rich)
- 6 days
Property
IgA
Values
- Least abundant (~0.001%)
- 188 kDa
- NO
- NO
- Mast cells, basophils, serum (trace)
- Allergic/anaphylactic reactions, parasitic infections (very high in parasites)
- 2–3 days (bound to mast cell longer)
Property
IgE
Values
- Trace (~0.01%)
- 184 kDa
- NO
- NO
- B cell surface (as receptor)
- B cell activation, least understood role
- 2–3 days
Property
IgD
Columns
- Antibody
- Abundance
- Molecular Weight
- Crosses Placenta
- First in Acute Infection
- Location
- Function
- Half-Life
Table Title
Immunoglobulin Comparison
Rows
Values
- Body makes own after INFECTION
- Actual pathogen exposure
- Slow (7–14 days)
- Long (years to lifetime)
- YES (strong)
- Immunity after chickenpox, measles, COVID-19
Property
Natural Active
Values
- Body makes own after VACCINE
- Attenuated/killed antigen, toxoid, subunit
- Slow (7–14 days, peak 2–4 weeks)
- Long (years to lifetime; varies by vaccine)
- YES (strong; booster reinforces)
- MMR, hepatitis B, tetanus toxoid, COVID-19 vaccine
Property
Artificial Active
Values
- Ready-made (MATERNAL)
- IgG across placenta; IgA/IgG in breast milk
- Immediate
- Temporary (6 months maternal IgG; varies for IgA)
- NO
- Newborn protected by maternal IgG; breastfed infant gets IgA
Property
Natural Passive
Values
- Ready-made (INJECTION)
- Immune serum, immunoglobulin, monoclonal antibody
- Immediate (hours)
- Temporary (2–6 weeks, depends on type)
- NO
- Tetanus immunoglobulin (TIG), hepatitis B Ig (HBIG), rabies Ig (RIG), antivenom
Property
Artificial Passive
Columns
- Type
- Source of Antibodies
- Method
- Onset
- Duration
- Memory
- Example
Table Title
Active vs Passive Immunity
Rows
Values
- Genetic defect; inherited; present from birth
- Another disease, treatment, or condition; develops over time
Property
Cause
Values
- Rare (~1 in 2000 births)
- Common (millions worldwide)
Property
Frequency
Values
- Infancy to childhood
- Any age (childhood to elderly)
Property
Age of onset
Values
- B cells (e.g., Bruton agammaglobulinemia), T cells (e.g., DiGeorge), both (e.g., SCID), or complement
- Often T cells initially (HIV → CD4 destruction) or neutrophils (chemo) or antibodies (malignancy)
Property
Affected cells/components
Values
- SCID, DiGeorge, Bruton agammaglobulinemia, selective IgA deficiency, complement deficiency
- HIV/AIDS, leukemia/lymphoma, chemotherapy, radiation, corticosteroids, splenectomy, malnutrition, aging
Property
Examples
Values
- Usually permanent (unless gene therapy/stem cell transplant)
- Often reversible if underlying cause treated (e.g., ART for HIV, recovery post-chemo)
Property
Reversibility
Values
- Without treatment, often fatal in infancy; SCID is now treatable with HSCT or gene therapy
- Depends on cause and treatment; HIV now manageable with ART; chemotherapy-induced is reversible
Property
Prognosis
Columns
- Feature
- Primary (Congenital)
- Secondary (Acquired)
Table Title
Primary vs Secondary Immunodeficiency
Rows
Values
- Usually localized or mild systemic (e.g., generalized urticaria, mild wheezing)
- Severe systemic (multiple organ systems: cardiovascular collapse, airway edema, bronchospasm)
Property
Systemic involvement
Values
- Normal to mildly reduced
- SEVERELY REDUCED (hypotensive, shock)
Property
Blood pressure
Values
- Mild wheeze, treatable with bronchodilator, minimal distress
- Stridor, laryngeal edema, severe bronchospasm, respiratory distress, possible airway obstruction
Property
Airway/respiratory
Values
- Tachycardia, stable BP
- Tachycardia, HYPOTENSION, syncope, SHOCK (distributive)
Property
Cardiovascular
Values
- Minutes to hours
- SECONDS to MINUTES (very rapid onset)
Property
Timing
Values
- Antihistamine (diphenhydramine), consider bronchodilator if wheezing
- EPINEPHRINE 0.3–0.5 mg IM (1:1000) IMMEDIATELY; airway support; IV fluids
Property
First-line treatment
Values
- 1–2 hours if resolved; discharge home if stable
- Minimum 4–8 hours (or longer) due to risk of biphasic reaction
Property
Observation period
Columns
- Feature
- Severe Allergic Reaction (Non-Anaphylactic)
- Anaphylaxis
Table Title
Anaphylaxis vs Severe Allergic Reaction
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