Podcast
Questions and Answers
Which type of hypersensitivity reaction is characterized by T-cell-mediated inflammation?
Which type of hypersensitivity reaction is characterized by T-cell-mediated inflammation?
- Type II hypersensitivity
- Type IV hypersensitivity (correct)
- Type I hypersensitivity
- Type III hypersensitivity
What is a common feature of Type I hypersensitivity reactions?
What is a common feature of Type I hypersensitivity reactions?
- Immune complexes deposit in tissues.
- T cells destroy pancreatic beta cells.
- IgG/IgM antibodies attack self-tissue.
- Mast cell degranulation occurs. (correct)
Which of the following is NOT a risk factor for Type IV hypersensitivity?
Which of the following is NOT a risk factor for Type IV hypersensitivity?
- Contact with certain chemicals like formaldehyde
- Infectious diseases like tuberculosis
- Exposure to allergens like poison ivy
- Blood transfusions (correct)
For which type of hypersensitivity is prior exposure indicated by a positive Mantoux test?
For which type of hypersensitivity is prior exposure indicated by a positive Mantoux test?
Which statement about Type II hypersensitivity is correct?
Which statement about Type II hypersensitivity is correct?
What initiates the production of IgE antibodies in Type I hypersensitivity reactions?
What initiates the production of IgE antibodies in Type I hypersensitivity reactions?
Which clinical manifestation is associated with Type I hypersensitivity reactions?
Which clinical manifestation is associated with Type I hypersensitivity reactions?
What is the mechanism of action behind Type II hypersensitivity reactions?
What is the mechanism of action behind Type II hypersensitivity reactions?
Which of the following conditions is an example of Type II hypersensitivity?
Which of the following conditions is an example of Type II hypersensitivity?
In Type I hypersensitivity, which substance is primarily released by mast cells upon re-exposure to an allergen?
In Type I hypersensitivity, which substance is primarily released by mast cells upon re-exposure to an allergen?
What are commonly associated risk factors for Type I hypersensitivity reactions?
What are commonly associated risk factors for Type I hypersensitivity reactions?
Which of the following best describes Type II hypersensitivity reactions?
Which of the following best describes Type II hypersensitivity reactions?
What is a key characteristic of Type I hypersensitivity reactions regarding their transmissibility?
What is a key characteristic of Type I hypersensitivity reactions regarding their transmissibility?
What is the primary cause of Type III Hypersensitivity?
What is the primary cause of Type III Hypersensitivity?
What occurs during the sensitization phase of Type IV Hypersensitivity?
What occurs during the sensitization phase of Type IV Hypersensitivity?
Which statement accurately describes the pathophysiology of Type III Hypersensitivity?
Which statement accurately describes the pathophysiology of Type III Hypersensitivity?
What type of agents can trigger Type IV Hypersensitivity?
What type of agents can trigger Type IV Hypersensitivity?
Which of the following autoimmune diseases is categorized under Type III Hypersensitivity?
Which of the following autoimmune diseases is categorized under Type III Hypersensitivity?
In Type IV Hypersensitivity, which cells are primarily involved in the delayed inflammatory response?
In Type IV Hypersensitivity, which cells are primarily involved in the delayed inflammatory response?
What kind of response is characterized by the recruitment of neutrophils in Type III Hypersensitivity?
What kind of response is characterized by the recruitment of neutrophils in Type III Hypersensitivity?
Flashcards
Type I hypersensitivity
Type I hypersensitivity
An immune response triggered by exposure to allergens, involving IgE antibodies binding to mast cells and leading to the release of histamine, leukotrienes, and prostaglandins.
Sensitization Phase
Sensitization Phase
The initial exposure to an allergen that leads to the production of IgE antibodies which bind to mast cells and basophils.
Re-exposure Phase
Re-exposure Phase
Re-exposure to the same allergen, triggering cross-linking of IgE on the surface of mast cells, leading to their degranulation and the release of inflammatory mediators.
Clinical Manifestations of Type I Hypersensitivity
Clinical Manifestations of Type I Hypersensitivity
Signup and view all the flashcards
Type II hypersensitivity
Type II hypersensitivity
Signup and view all the flashcards
Antibody-Mediated Destruction
Antibody-Mediated Destruction
Signup and view all the flashcards
Graves' disease
Graves' disease
Signup and view all the flashcards
Myasthenia gravis
Myasthenia gravis
Signup and view all the flashcards
Autoimmune Disease
Autoimmune Disease
Signup and view all the flashcards
Risk Factor for Autoimmune Disease
Risk Factor for Autoimmune Disease
Signup and view all the flashcards
Immune Complexes
Immune Complexes
Signup and view all the flashcards
Cytokine Release in Type IV Hypersensitivity
Cytokine Release in Type IV Hypersensitivity
Signup and view all the flashcards
What is Type 1 diabetes?
What is Type 1 diabetes?
Signup and view all the flashcards
What does a positive TB skin test mean?
What does a positive TB skin test mean?
Signup and view all the flashcards
What is Type IV hypersensitivity?
What is Type IV hypersensitivity?
Signup and view all the flashcards
What is Type II hypersensitivity?
What is Type II hypersensitivity?
Signup and view all the flashcards
How can tuberculosis trigger Type IV hypersensitivity?
How can tuberculosis trigger Type IV hypersensitivity?
Signup and view all the flashcards
Study Notes
Hypersensitivity Reactions
- Hypersensitivity reactions are immune responses that cause harm rather than benefit.
- Four main types of hypersensitivity reactions exist: Type I, Type II, Type III, and Type IV.
Type I Hypersensitivity (Immediate/Allergic Reactions)
- Cause: Exposure to allergens like pollen, pet dander, food, insect venom, or medications.
- Pathophysiology:
- Sensitization phase: Initial exposure triggers IgE antibody production, binding to mast cells and basophils.
- Re-exposure: Subsequent exposure causes cross-linking of IgE, triggering mast cell degranulation and release of histamine, leukotrienes, prostaglandins.
- This leads to increased vascular permeability, smooth muscle contraction, and mucus secretion.
- Clinical Manifestations: Urticaria (hives), allergic rhinitis (hay fever), asthma, and anaphylaxis.
- Transmission: Not transmissible; a response triggered by exposure to allergens.
- Risk Factors: Genetic predisposition to atopy (family history of allergies, asthma, or eczema), environmental exposure to allergens, and occupation-related exposure.
Type II Hypersensitivity (Cytotoxic Reactions)
- Cause: Autoimmune disorders (e.g., Graves' disease, Myasthenia gravis) and blood transfusion reactions where the body's immune system targets its own tissues (self-antigens) or foreign antigens.
- Pathophysiology:
- Antibodies (IgG or IgM) bind to antigens on cell surfaces.
- This leads to opsonization and phagocytosis by macrophages.
- Complement system activation causes cell lysis and death.
- Examples: Graves' disease (antibodies bind to TSH receptors), Myasthenia gravis (antibodies block acetylcholine receptors).
- Transmission: Not transmissible; a result of the body's immune response to self or foreign antigens.
Type III Hypersensitivity (Immune Complex-Mediated)
- Cause: Formation of immune complexes (antigen-antibody complexes) that deposit in tissues, leading to inflammation.
- Pathophysiology:
- Circulating immune complexes become trapped in blood vessels or tissues.
- Complement activation recruits neutrophils, releasing enzymes causing tissue damage.
- Inflammation and necrosis result in organ damage.
- Examples: Systemic lupus erythematosus (SLE), rheumatoid arthritis (RA).
- Transmission: Not transmissible; a result of the body's immune response to self or foreign antigens.
- Risk Factors: Autoimmune diseases (e.g., SLE and RA), chronic infections.
Type IV Hypersensitivity (Delayed/Cell-Mediated)
- Cause: Exposure to environmental antigens (e.g., poison ivy), medications, or infectious agents.
- Pathophysiology:
- Sensitization phase: Memory T cells are generated after initial exposure.
- Re-exposure: Activates memory T cells, releasing cytokines like IFN-γ and TNF-α.
- Delayed inflammatory response leads to macrophage recruitment and tissue damage.
- Examples: Contact dermatitis (e.g., poison ivy).
- Transmission: Not transmissible; a result of T-cell-mediated immune responses.
- Risk Factors: Exposure to allergens, topical medications, chemicals like formaldehyde, and infections (e.g., Tuberculosis).
Studying That Suits You
Use AI to generate personalized quizzes and flashcards to suit your learning preferences.