Podcast
Questions and Answers
Which of the following is the primary immunoglobulin involved in Type I hypersensitivity reactions?
Which of the following is the primary immunoglobulin involved in Type I hypersensitivity reactions?
Which physiological response is NOT a direct result of the release of mediators during a Type I hypersensitivity reaction?
Which physiological response is NOT a direct result of the release of mediators during a Type I hypersensitivity reaction?
A patient experiencing a severe Type I hypersensitivity reaction requires immediate treatment. Which medication would be the priority?
A patient experiencing a severe Type I hypersensitivity reaction requires immediate treatment. Which medication would be the priority?
What is the primary mechanism involved in Type II hypersensitivity reactions?
What is the primary mechanism involved in Type II hypersensitivity reactions?
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Which of the following examples best illustrates a Type II hypersensitivity reaction?
Which of the following examples best illustrates a Type II hypersensitivity reaction?
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A patient with allergic rhinitis experiences symptoms related to Type I hypersensitivity. Which combination of clinical manifestations would be most consistent with this type of reaction?
A patient with allergic rhinitis experiences symptoms related to Type I hypersensitivity. Which combination of clinical manifestations would be most consistent with this type of reaction?
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In a Type II hypersensitivity reaction, which molecules are principally responsible for targeting and damaging cells?
In a Type II hypersensitivity reaction, which molecules are principally responsible for targeting and damaging cells?
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Which statement correctly links a mediator to its effect in a Type I hypersensitivity reaction?
Which statement correctly links a mediator to its effect in a Type I hypersensitivity reaction?
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Which hypersensitivity reaction involves the formation and deposition of antigen-antibody complexes in tissues, leading to inflammation?
Which hypersensitivity reaction involves the formation and deposition of antigen-antibody complexes in tissues, leading to inflammation?
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In Type IV hypersensitivity reactions, which cells primarily mediate the delayed immune response?
In Type IV hypersensitivity reactions, which cells primarily mediate the delayed immune response?
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What is the primary mechanism of tissue damage in Type V hypersensitivity?
What is the primary mechanism of tissue damage in Type V hypersensitivity?
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Which of the following is not a symptom of rheumatoid arthritis?
Which of the following is not a symptom of rheumatoid arthritis?
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What is the primary treatment approach for Goodpasture's syndrome?
What is the primary treatment approach for Goodpasture's syndrome?
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What is the primary immunological mechanism in Myasthenia gravis?
What is the primary immunological mechanism in Myasthenia gravis?
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How does plasmapheresis aid in managing hypersensitivity reactions?
How does plasmapheresis aid in managing hypersensitivity reactions?
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What is the crucial primary preventive strategy for patients with contact dermatitis due to latex allergy?
What is the crucial primary preventive strategy for patients with contact dermatitis due to latex allergy?
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In the context of nursing care, what is the first priority intervention for managing hypersensitivity reactions?
In the context of nursing care, what is the first priority intervention for managing hypersensitivity reactions?
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What is the underlying mechanism leading to hyperthyroidism in Graves’ disease?
What is the underlying mechanism leading to hyperthyroidism in Graves’ disease?
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Flashcards
Autoimmune disease
Autoimmune disease
Immune system attacks own tissues due to mistaken identity.
Goodpasture's syndrome
Goodpasture's syndrome
Antibodies mistakenly target lung and kidney basement membranes, causing inflammation and damage.
Myasthenia gravis
Myasthenia gravis
Autoantibodies bind to acetylcholine receptors, impairing muscle function leading to weakness.
Immune complex hypersensitivity
Immune complex hypersensitivity
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Systemic Lupus Erythematosus (SLE)
Systemic Lupus Erythematosus (SLE)
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Rheumatoid Arthritis (RA)
Rheumatoid Arthritis (RA)
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Serum sickness
Serum sickness
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Delayed-Type Hypersensitivity
Delayed-Type Hypersensitivity
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Contact dermatitis
Contact dermatitis
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Stimulatory Hypersensitivity
Stimulatory Hypersensitivity
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Hypersensitivity Reactions
Hypersensitivity Reactions
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Type I Hypersensitivity (Immediate Hypersensitivity)
Type I Hypersensitivity (Immediate Hypersensitivity)
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Mechanism of Type I Hypersensitivity
Mechanism of Type I Hypersensitivity
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Anaphylaxis
Anaphylaxis
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Type II Hypersensitivity (Cytotoxic Hypersensitivity)
Type II Hypersensitivity (Cytotoxic Hypersensitivity)
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Blood Transfusion Reactions
Blood Transfusion Reactions
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Epinephrine for Anaphylaxis
Epinephrine for Anaphylaxis
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Allergen Avoidance
Allergen Avoidance
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Study Notes
Hypersensitivity Types
- Hypersensitivity reactions are overreactions of the immune system to antigens.
- Five types exist, each with unique pathophysiology, symptoms, and treatments.
Type I: Immediate Hypersensitivity
- Mechanism: IgE-mediated rapid allergic response. Initial exposure creates IgE antibodies which bind to mast cells. Re-exposure triggers mast cell degranulation, releasing mediators (histamine, prostaglandins, leukotrienes).
- Effects: Smooth muscle contraction, vasodilation, bronchoconstriction, increased vascular permeability causing allergic symptoms.
- Epidemiology: Allergic rhinitis affects ~11% U.S. population. Anaphylaxis (most severe) has a 1-2% lifetime prevalence, increasing in children.
- Common Triggers: Food, medications, insect stings, latex.
- Local Reactions (e.g., allergic rhinitis): Sneezing, nasal discharge, sinus pressure, itchy/watery eyes.
- Systemic Reactions (e.g., anaphylaxis): Dyspnea, wheezing, rash, nausea, vomiting, hypotension, tachycardia, angioedema. Severe cases lead to bronchospasm, airway obstruction, anaphylactic shock.
- Management: Mild cases use antihistamines & decongestants. Severe reactions require immediate IM epinephrine (relaxes bronchioles, constricts vessels), oxygen, corticosteroids (e.g., methylprednisolone), and bronchodilators (e.g., albuterol). Nursing care involves monitoring, removing allergen, administering meds, and teaching about EpiPen use and avoidance.
Type II: Cytotoxic Hypersensitivity
- Mechanism: Antibody-mediated; IgG and IgM antibodies target cells, activating complement or antibody-dependent cytotoxicity, leading to cell lysis or dysfunction.
- Examples:
- Blood transfusion reactions (mismatched blood): hemolysis, acute renal failure, systemic inflammation.
- Goodpasture's syndrome: autoimmune attack on lung and kidney basement membranes, leading to glomerulonephritis and pulmonary hemorrhage.
- Myasthenia gravis: autoantibodies bind to acetylcholine receptors, impairing neuromuscular function and causing muscle weakness.
- Management: Remove causative agent (e.g., discontinue mismatched blood). Plasmapheresis (removes harmful antibodies). Corticosteroids, immunosuppressants, sometimes dialysis or renal transplantation (for Goodpasture's syndrome).
Type III: Immune Complex Hypersensitivity
- Mechanism: Antigen-antibody complexes deposit in tissues, causing inflammation and tissue damage. Immune complexes are slow to clear.
- Examples:
- Systemic lupus erythematosus (SLE): Autoimmune complexes lodge in organs, causing inflammation (vasculitis, nephritis, arthritis, neurological issues).
- Rheumatoid arthritis (RA): Complexes in joints leading to chronic inflammation and destruction.
- Serum sickness: Reaction to proteins (in medications or antiserum), causing fever, rash, joint pain, angioedema.
- Management: Remove causative agent. Symptomatic relief with antihistamines, corticosteroids. Severe cases may need epinephrine or immunosuppressants.
Type IV: Delayed-Type Hypersensitivity
- Mechanism: T-lymphocyte mediated, not antibody-mediated. Delayed response (24-72 hours after exposure). Involves macrophage activation and tissue destruction.
- Examples:
- Contact dermatitis (poison ivy, latex): localized redness, itching, swelling.
- Mantoux test (Tuberculosis): localized wheal and flare reaction.
- Latex allergy: Delayed reaction, or sometimes immediate (Type I).
- Management: Prevent exposure. Mild reactions use antihistamines or topical corticosteroids. Severe reactions may need epinephrine, oxygen, IV corticosteroids. Patient education (latex-free precautions, EpiPen).
Type V: Stimulatory Hypersensitivity
- Mechanism: Autoantibodies excessively stimulate cell-surface receptors, leading to overactive cell function.
- Example: Graves' disease: autoantibodies bind to TSH receptors, increasing thyroid hormone production (causing hyperthyroidism: tachycardia, weight loss, heat intolerance).
- Management: Medications to block hormone production (e.g., antithyroid drugs), supportive care for hyperthyroid symptoms.
Nursing Care & Interventions
- General Focus: Prompt recognition, removal of offending agent, prevention of complications.
- Key Interventions:
- Monitoring: Respiratory status, vital signs, and systemic reaction symptoms.
- Emergency Preparedness: Immediate access to emergency medications (e.g., epinephrine, corticosteroids), resuscitation equipment.
- Education: Teach patients to recognize early symptoms, avoid triggers, use EpiPens (if applicable), and wear Medic Alert bracelets.
Conclusion
- Hypersensitivity reactions range from mild allergies to life-threatening anaphylaxis.
- Effective management depends on understanding pathophysiology, prompt intervention, and prevention strategies, tailored to individual needs.
- Nursing care is crucial for monitoring, treatment and education.
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Description
This quiz covers the various types of hypersensitivity reactions, focusing on the mechanisms, effects, and epidemiology of Type I: Immediate Hypersensitivity. Learn about the common triggers and symptoms associated with these immune responses. Ideal for students studying immunology or pathology.
