IMS CH 33

Immunoglobulins (antibodies)
- Five main classes: IgG, IgA, IgM, IgD, IgE.
- IgE is the antibody class that mediates most allergic (hypersensitivity) reactions.
Role of lymphocyte subsets
- B-cells: Produce antigen-specific antibodies (e.g., IgE) after stimulation.
- T-cells: Assist B-cells, secrete cytotoxic substances, activate macrophages, and help clear antigen–antibody debris.
Chemical mediators involved in allergy (released from mast cells / basophils when IgE cross-links with antigen)
- Histamine, leukotrienes, prostaglandins, bradykinin, platelet-activating factor, cytokines, etc.
- Responsible for vasodilation, increased capillary permeability, bronchoconstriction, pruritus, mucous secretion, and edema.

Allergy: An exaggerated immune response to otherwise harmless environmental antigens (pollens, dust, mites, dander, foods, drugs, insect venom, latex, etc.).
Clinical spectrum ranges from mild (itchy/watery eyes, sneezing, local rash) to life-threatening systemic anaphylaxis, angioedema, bronchoconstriction, or circulatory collapse.
Four classic types of hypersensitivity (Gell & Coombs classification):
1. Type I – Anaphylactic / Immediate (IgE-mediated)
2. Type II – Cytotoxic (IgG or IgM antibodies against cell-bound antigen)
3. Type III – Immune-Complex (IgG/IgM complexes deposited in tissues)
4. Type IV – Delayed / Cell-mediated (T-cell driven)

Triggered seconds–minutes after re-exposure to antigen; IgE on mast cells/basophils cross-links → degranulation.
Classic examples:
- Allergic rhinitis (hay fever)
- Systemic anaphylaxis (foods, drugs, insect stings)
- Angioedema (often ACE-inhibitor–induced): swelling of lips, face, tongue, larynx → airway threat.
Pathophysiology cascade
- Widespread vasodilation → ↓ venous return & ↓ cardiac output.
- Bronchoconstriction & laryngeal edema → stridor / respiratory failure.
Emergency management priorities
1. Airway & gas exchange: Oxygen, prepare for intubation; if tongue/larynx too swollen, perform tracheostomy.
2. Medications
- Epinephrine (EpiPen) $1:1000$ IM into anterolateral thigh (vastus lateralis).
- Diphenhydramine (antihistamine), corticosteroids, β2-agonists, leukotriene antagonists.
1. Prevention: Allergen avoidance, carry EpiPen, wear medical alert identification, mask during high-pollen seasons, avoid pets if dander-allergic.

Antibodies bind to antigen on patient’s own cells → complement activation & cell lysis.
Representative conditions:
- Myasthenia gravis (antibodies against acetylcholine receptors).
- Goodpasture syndrome: Auto-antibodies against glomerular basement membrane; damages kidneys & lungs.
  • Clinical: hematuria, glomerulonephritis, pulmonary hemorrhage/dyspnea.
  • Treatment: high-dose corticosteroids, plasmapheresis.
- Pernicious anemia (anti-intrinsic-factor/ parietal-cell antibodies).
- Hemolytic transfusion reactions (ABO incompatibility).

Soluble antigen–antibody complexes deposit in tissues → complement-mediated inflammation.
Key diseases:
- Rheumatoid arthritis (RA) – joints, skin.
- Systemic lupus erythematosus (SLE) – skin, joints, kidneys (lupus nephritis).
- Sjogren’s syndrome (often overlaps with RA & fibromyalgia):
  • Excessive dryness of eyes (xerophthalmia), mouth (xerostomia), nasal mucosa, vagina.
  • Symptom relief: artificial tears, ocular lubricants, artificial saliva preparations, vaginal moisturizers.

Onset 24–72 h post-exposure; mediated by sensitized T-lymphocytes.
Prototype examples:
- Contact dermatitis (poison ivy, nickel, cosmetics, latex in some cases).
- Tuberculin skin test (PPD) – induration = positive.
- Hashimoto’s thyroiditis, Type 1 diabetes mellitus (islet-cell destruction).
- Local response to insect stings (contrast with systemic Type I reactions).

Skin testing: prick / intradermal panels on forearm or back to identify specific allergens.
• Multiple small needle pricks; observe for wheal & flare.
Laboratory tests
- Complete blood count (CBC): check eosinophil count (often elevated in atopy).
- Total IgE level.
- Radioallergosorbent test (RAST) / ImmunoCAP for specific IgE.

Pharmacologic options
- Antihistamines (e.g., diphenhydramine, cetirizine).
- Decongestants.
- Corticosteroids (systemic or inhaled/nasal).
- Leukotriene antagonists (montelukast).
EpiPen education
- Carry at all times; inspect expiration date.
- Inject through clothing if necessary into mid-outer thigh; hold $\ge$ 3 seconds.
- Seek emergency care after use (rebound phenomena possible).
Airway management hierarchy
1. High-flow O₂.
2. Endotracheal intubation if feasible.
3. If oropharyngeal edema precludes intubation → emergent surgical airway (tracheostomy).
Anxiety reduction: Calm reassurance; feeling of impending doom common.

True latex allergy can provoke anaphylaxis from minimal exposure (gloves, catheters, balloons).
Clinical signs: localized or systemic urticaria, erythema, itching, angioedema, bronchospasm.
High-risk cross-reactive foods (contain proteins similar to latex antigens)
- HIGH: banana, avocado, chestnut, kiwi.
- MODERATE: apple, carrot, celery, papaya, potato, tomato, melons.
- LOW: cherries, figs, grapes, pineapple, strawberry, wheat, hazelnut, peanut.
Patient teaching: Avoid offending foods; use non-latex gloves (nitrile, vinyl) and equipment.

Sequence of an acute inflammatory response: injury → vasodilation → capillary permeability ↑ → edema → chemotaxis & cellular infiltration → resolution or chronic inflammation.
Simple measure: Pollen-allergic individuals should wear masks outdoors during high-count days.
ACE-inhibitors are a common drug class precipitating angioedema; monitor new hypertensive patients for lip/tongue swelling.
Always treat any unknown rash + respiratory symptoms post med/food exposure as potential anaphylaxis until ruled out.