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Related Concept Videos

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

58
Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
58
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

40
Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
40
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

43
Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
43
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

48
Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
48
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

38
Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial...
38
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

44
Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin,...
44

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Rivaroxaban-Induced Hypersensitivity Syndrome

Charles-Olivier Chiasson1, Arnaud Canneva2, François-Olivier Roy3

  • 1, PharmD, MSc, was, at the time this manuscript was originally prepared, a Pharmacy Resident at the McGill University Health Centre and a student in the Faculty of Pharmacy, Université de Montreal, Montréal, Quebec. He is now a Pharmacist at the Centre hospitalier universitaire Sainte-Justine, Montréal, Quebec.

The Canadian Journal of Hospital Pharmacy
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PubMed
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No abstract available in PubMed .

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