Hypersensitivity
Overview of Innate and Adaptive Immunity
Innate immunity: normal body defense mechanisms
Adaptive immunity: recognition and response to threats
Innate Immunity
First Line of Defense: Barriers against pathogens
Skin and mucous membranes
Second Line of Defense: Internal defenses
Phagocytic cells, inflammation, fever
Inflammation: Body's response to injury
Acute vs. chronic inflammation
Wound Healing: Repair mechanisms of the body
Adaptive Immunity
Immune system evolution from neonate to geriatric stages
Recognition of specific threats
Importance of prior knowledge from pathophysiology courses
Alterations in Immune and Inflammatory Responses
Exaggerated immune reactions
Misdirected immune actions (Autoimmunity)
Poor immune response (Immunodeficiency)
Hypersensitivity Reactions
Definition: Exaggerated immune response causing damage to the host
Sensitization: Initial exposure that leads to possible reactions upon re-exposure
Four Classifications of Hypersensitivity Reactions:
Type I: Immediate
Type II: Tissue-specific
Type III: Immune complex mediated
Type IV: Delayed hypersensitivity
Type I Hypersensitivity (IgE Mediated)
Definition: Exaggerated response to environmental antigens (allergens)
Examples: Hay fever, asthma, eczema, food allergies
Mechanism:
IgE binds to mast cells, leading to degranulation and release of histamine
Symptoms: Increased vascular permeability, bronchial smooth muscle contraction, gastric acid secretion
Anaphylaxis: Most severe complication; life-threatening
Symptoms include itching, erythema, systemic response with vasodilation, and respiratory distress
Common triggers: Bee stings, peanuts, eggs, shellfish
Type II Hypersensitivity (Tissue-Specific)
Definition: Reaction to specific tissues due to antibodies against antigens on cell membranes
Examples:
Autoimmune thrombocytopenia (platelets)
Graves' disease (thyroid stimulating hormone receptor)
Goodpasture syndrome (kidney membrane destruction)
Transfusion reactions due to ABO mismatching
Mechanism:
Cell lysis via membrane attack complexes formed by antibodies and complement activation
Consequences include hemolytic anemia and organ dysfunction
Type III Hypersensitivity (Immune Complex Mediated)
Definition: Immune complexes deposit in tissues
Examples: Serum sickness, Raynaud's phenomenon, lupus, rheumatoid arthritis
Mechanism:
Antigen-antibody complexes activate complement, resulting in localized inflammation
Symptoms vary based on affected tissues: arthritis, vasculitis, glomerulonephritis
Type IV Hypersensitivity (Delayed)
Definition: T-cell mediated responses that take days to manifest
Examples: Contact dermatitis, Steven Johnson syndrome, drug reactions
Mechanism:
Activation of T cells and macrophages leads to tissue damage
Granulomatous responses can occur in conditions like tuberculosis and sarcoidosis
Disorders Related to Hypersensitivity
Allergies: hypersensitivity to environmental antigens
Genetic predisposition must be considered
Symptoms vary but can include conjunctivitis, urticaria, asthma
Testing includes skin tests and measuring IgE levels
Desensitization can reduce life-threatening reactions
Autoimmunity:
Breakdown of immune tolerance
Examples: lupus, MS, celiac disease, myasthenia gravis
Increased prevalence in females; family history often involved
Alloimmunity: Immune response against tissues from another individual
Examples: Transplant rejection, blood transfusion reactions
Transfusion reactions can be immediate or delayed
Transfusion and Transplant Reaction Mechanisms
ABO System:
A and B antigens determine blood types; universal donors and recipients
IgM antibodies responsible for most transfusion reactions
Rh Factor:
Rh positive and negative categorization based on D antigen
Hemolytic disease of the newborn: Rh incompatibility leading to anemia in infants
Transplant Rejection:
Can be hyperacute (minutes), acute (days to months), or chronic (months to years)
Managed through HLA matching and immunosuppressive therapy to prevent rejection reactions
Autoimmunity Example: Systemic Lupus Erythematosus (SLE)
Characteristics: Production of autoantibodies against a range of self-antigens
Symptoms: Skin rashes, joint pain, organ involvement (kidneys), potential for renal failure
Management: Focus on minimizing systemic effects; treatment can include anti-inflammatories, steroids, and immunosuppressants
Conclusion
Understanding hypersensitivity reactions is crucial for clinical practice
Early recognition of symptoms and appropriate interventions can prevent severe outcomes
Collaboration across healthcare disciplines enhances patient safety and care in allergic, autoimmune, and alloimmune conditions.