Hypersensitivity Diseases Quiz

Hypersensitivity Disorders

• Hypersensitivity diseases are caused by immune responses
• This term is derived from the idea of excessive or aberrant immune responses to an antigen
• Immune responses can be inadequately controlled or inappropriately targeted to host tissues, or triggered by harmless commensal microorganisms or environmental antigens.

Causes of Hypersensitivity Diseases

• Immune responses that result in hypersensitivity are sometimes inadequately controlled, inappropriately targeted to host tissues, or triggered by commensal microorganisms or environmental antigens that are usually harmless.

Types of Hypersensitivity Diseases

• Type I (Immediate Hypersensitivity): Characterized by a rapid, IgE antibody- and mast cell-mediated response resulting in vascular and smooth muscle reaction, often followed by inflammation.
  • Occurs when individuals encounter certain foreign antigens previously exposed to.
  • Also called allergy or atopy.
  • Involves the production of IgE antibodies against environmental antigens and the subsequent binding of IgE to mast cells in various tissues
  • Tissue injury occurs due to mast cell mediator release in response to allergens
    • Early phase is rapid mediator release, including histamine
    • Late phase reaction involves cytokine production, recruiting and activating other immune cells (neutrophils, eosinophils). These lead to more tissue inflammation and injury.
• Type II (Antibody-mediated Diseases): Mediated by antibodies other than IgE, affecting cells or tissues in two ways:
  • Damage occurs by antibodies directed against cell or tissue antigens, damaging them or impairing function
  • These diseases are often non-systemic
• Type III (Immune Complex-mediated Diseases):
  • Antibodies against soluble antigens may form complexes
  • Complexes can deposit in blood vessels and cause inflammation or tissue damage
  • Systemic diseases often result, such as serum sickness and Arthus reactions
• Type IV (T Cell-mediated Diseases):
  • The primary mechanism involves:
    • delayed-type hypersensitivity (DTH): a form of injurious cytokine-mediated inflammatory reaction from the activation of T cells, particularly CD4+ T cells.
    • T-cell mediated cytotoxicity
• Mechanisms of Tissue Injury:
  • Results from the products of activated neutrophils and macrophages that exhibit increased lysosomal enzymes, reactive oxygen species, nitric oxide, and proinflammatory cytokines
  • Inflammation associated with T cell-mediated diseases is typically chronic, though bouts of acute inflammation may be superimposed on a chronic inflammation background
  • Many organ-specific autoimmune diseases are caused by interactions between autoreactive T cells and self-antigens that lead to the release of cytokines and inflammation. T-cell reactions against microbes/foreign antigens may lead to inflammation and tissue injury associated with delayed hypersensitivity

Questions about Hypersensitivity

• Factors contributing to the development of hypersensitivity diseases
• Immunologic mechanisms causing tissue injury and functional abnormalities in different types of hypersensitivity disorders
• The major clinical and pathological features of these diseases and the principles underlying treatment of hypersensitivity diseases

Common Hypersensitivity Diseases

• Hay Fever: Inhaled allergens (like ragweed pollen) trigger histamine production in nasal mucosa. Leading to mucosal edema, leukocyte infiltration, and mucus secretion causing breathing difficulties. Late-phase reaction can lead to nasal polyps.
• Food Allergies: Ingested allergens trigger mast cell degranulation, release of histamine causing increased peristalsis. Leads to nausea, vomiting, increased mucous secretion, urticaria, and anaphylaxis
• Allergy Presentations in Skin: Includes urticaria (hives) and eczema.
• Bronchial Asthma: Reversible and intermittent obstruction of airways is a hallmark, accompanied by chronic eosinophilic inflammation of bronchi and smooth muscle hypertrophy. Increased reaction to bronchoconstrictors; Inhaled allergens stimulate bronchial mast cells, leading to mediator release, including leukotrienes, resulting in repeated bronchial constriction and airway obstruction. In chronic asthma, excessive mucous secretion and hyperreactive smooth muscles are common
• Non-IgE Mediated Asthma: Some asthma cases are not associated with IgE production, but all result from mast cell activation (cold, exercise trigger).
• Anaphylaxis: The most severe form of immediate hypersensitivity (systemic). Characterized by widespread edema in numerous tissues, including the larynx, accompanied by low blood pressure. Caused by widespread mast cell degranulation in response to a systemic antigen. Dangerous due to the sudden drop in blood pressure and airway obstruction, which requires immediate intervention.

Possible Treatment

• Targeting inhibiting mast cell degranulation
• Antogonizing the effects of mast cell mediators
• Reducing inflammation

Allergens

• The antigens that elicit immediate hypersensitivity are frequently common environmental proteins and chemicals that modify proteins.
• Allergens are structurally distinct molecules.
• Important characteristics are repeated exposure and unlike microbes, they do not generally stimulate the innate immune response.
• Allergens do not stimulate innate immunity, possess no distinct specificity, and they are typically glycosylated with low molecular weight and high solubility. Some have enzymatic activity and are usually proteins or polysaccharides attached to self-proteins (hapten-carrier complexes).

Common Treatment

• Antihistamines: Used to treat hay fever
• Bronchodilators and inhaled corticosteroids: Used to treat asthma
• Epinephrine: Used to treat anaphylaxis.
• Desensitization: Repeated administration of small doses of allergens.

Test your knowledge on hypersensitivity diseases and their underlying mechanisms. This quiz covers various types of hypersensitivity, including IgE-mediated reactions and delayed-type responses. Understand the clinical features and treatment principles associated with these immunologic disorders.