Daily MCQs test - hypersensitivity reaction pathology

Type 1 hypersensitivity is an exaggerated immune response that occurs when the immune system overreacts to harmless substances, known as allergens, leading to the release of inflammatory mediators. This type of hypersensitivity is also known as immediate hypersensitivity because the reaction occurs rapidly after exposure to the allergen. It is the most common type of allergic reaction. Here's how Type 1 hypersensitivity occurs:
1. Sensitization:The first exposure to an allergen sensitizes the immune system. Antigen-presenting cells (APCs) process the allergen and present its fragments to helper T cells (Th2 cells) in the context of major histocompatibility complex II (MHC II) molecules. Th2 cells recognize the allergen as foreign and activate B cells to produce specific immunoglobulin E (IgE) antibodies against the allergen.
2. IgE Production:B cells, stimulated by Th2 cells, undergo class switching to produce IgE antibodies instead of the usual IgM or IgG antibodies. These IgE antibodies have high affinity for receptors on the surface of mast cells and basophils.
3. Allergen Re-exposure:Upon subsequent exposure to the same allergen, it binds to the IgE antibodies on the surface of mast cells and basophils.
4. Degranulation:The cross-linking of IgE-bound receptors by the allergen triggers the release of inflammatory mediators from mast cells and basophils. These mediators include histamine, leukotrienes, prostaglandins, and cytokines.
5. Inflammatory Response:The released inflammatory mediators cause various allergic symptoms, depending on the site of exposure. Common manifestations of Type 1 hypersensitivity include:- Respiratory: Sneezing, runny or itchy nose, nasal congestion, coughing, wheezing, and asthma.- Skin: Itching, hives (urticaria), redness, and swelling (angioedema).- Gastrointestinal: Abdominal pain, nausea, vomiting, and diarrhea.
Examples of Type 1 hypersensitivity reactions include allergic rhinitis (hay fever), allergic asthma, allergic conjunctivitis, atopic dermatitis (eczema), and anaphylaxis, a severe and potentially life-threatening allergic reaction that involves systemic release of inflammatory mediators, leading to a rapid drop in blood pressure, difficulty breathing, and other serious symptoms.
Management of Type 1 hypersensitivity involves identifying and avoiding allergens whenever possible. Antihistamines, corticosteroids, and other medications may be used to relieve symptoms during allergic reactions. In severe cases, individuals at risk for anaphylaxis may carry epinephrine auto-injectors to quickly counteract the allergic response.
Overall, Type 1 hypersensitivity is an immune-mediated reaction that involves the production of IgE antibodies and the release of inflammatory mediators, leading to allergic symptoms. It is essential for individuals with known allergies to be aware of potential triggers and take appropriate precautions to manage their condition effectively.

Type 2 hypersensitivity is one of the four types of hypersensitivity reactions that occur due to an exaggerated immune response against self-antigens or foreign antigens. In Type 2 hypersensitivity, the immune system produces antibodies that target antigens located on the surface of host cells or tissues. This leads to the destruction of the affected cells or tissues by various immune effector mechanisms. The main mechanisms involved in Type 2 hypersensitivity are antibody-dependent cellular cytotoxicity (ADCC), complement activation, and phagocytosis. Here's a closer look at Type 2 hypersensitivity:

1. Mechanism:

- The immune system recognizes a specific antigen on the surface of host cells or tissues as foreign or abnormal.

- B cells are activated and produce antibodies, mainly IgG or IgM, against the target antigens.

- These antibodies bind to the antigens, forming antigen-antibody complexes on the cell surface.

2. Effector Mechanisms:

- ADCC: Antibodies bound to the cell surface can attract natural killer (NK) cells or other cytotoxic cells. The NK cells recognize the Fc portion of the bound antibodies and release cytotoxic granules, leading to the destruction of the targeted cell.

- Complement Activation: The antigen-antibody complexes can activate the complement system, resulting in the formation of the membrane attack complex (MAC). The MAC leads to the destruction of the cell membrane and lysis of the targeted cell.

- Phagocytosis: Opsonization occurs when the antibodies coat the target cell, making it more susceptible to phagocytosis by macrophages or neutrophils. The phagocytic cells engulf and destroy the opsonized cell.

3. Clinical Examples:

Type 2 hypersensitivity can manifest in various autoimmune diseases and immune-mediated disorders. Some examples include:

- Hemolytic anemia: Destruction of red blood cells due to autoantibodies targeting red blood cell antigens.

- Myasthenia gravis: Antibodies target and interfere with acetylcholine receptors at the neuromuscular junction, leading to muscle weakness and fatigue.

- Goodpasture's syndrome: Autoantibodies target the basement membrane of the kidneys and lungs, leading to glomerulonephritis and pulmonary hemorrhage.

It's important to note that Type 2 hypersensitivity is different from Type 1 hypersensitivity (immediate hypersensitivity) in which IgE antibodies trigger an immediate allergic response. In Type 2 hypersensitivity, the response is mediated by IgG or IgM antibodies and typically takes longer to develop.

Overall, Type 2 hypersensitivity reactions can lead to tissue damage and contribute to the pathogenesis of various autoimmune diseases and immune-mediated disorders. The reactions are complex and can involve multiple effector mechanisms, leading to a range of clinical manifestations depending on the targeted cells or tissues.

Type 3 hypersensitivity is one of the four types of hypersensitivity reactions in the immune system. In this type of hypersensitivity, immune complexes are formed when antibodies bind to antigens, resulting in their deposition in various tissues and organs. The deposition of immune complexes triggers an inflammatory response, leading to tissue damage and inflammation. Here's how Type 3 hypersensitivity occurs:

1. Antigen-Antibody Complex Formation:

After exposure to an antigen (usually a foreign substance or a self-antigen), the immune system produces antibodies (IgG or IgM) in response to the antigen. The antibodies bind to the antigen, forming immune complexes.

2. Immune Complex Deposition:

The immune complexes can circulate in the bloodstream and may deposit in various tissues, such as the blood vessels, joints, kidneys, skin, and other organs. The immune complexes can become trapped in these tissues, initiating an inflammatory response.

3. Activation of Complement System:

The deposited immune complexes can activate the complement system, leading to the formation of membrane attack complexes (MACs) and the release of pro-inflammatory molecules. The complement activation further amplifies the inflammatory response.

4. Inflammation and Tissue Damage:

The deposition of immune complexes and complement activation trigger an inflammatory response, leading to the recruitment of immune cells such as neutrophils, macrophages, and other inflammatory mediators. These immune cells release cytokines and enzymes that cause tissue damage, leading to various clinical manifestations.

Clinical Examples of Type 3 Hypersensitivity:

1. Systemic Lupus Erythematosus (SLE):

In SLE, immune complexes are formed against self-antigens, such as nuclear components (e.g., DNA, RNA, histones). The immune complexes can deposit in multiple organs, leading to symptoms like joint pain, skin rash (butterfly rash), kidney damage (glomerulonephritis), and other systemic manifestations.

2. Rheumatoid Arthritis (RA):

RA is characterized by the formation of immune complexes involving antibodies against components of joint tissues, such as rheumatoid factor (IgM antibodies against IgG). Immune complex deposition in the synovium of joints leads to chronic inflammation, joint destruction, and pain.

3. Serum Sickness:

Serum sickness can occur as a result of the administration of foreign proteins (e.g., from animal serum or certain medications). Immune complexes form and deposit in various tissues, leading to symptoms like fever, rash, joint pain, and lymph node enlargement.

Treatment of Type 3 Hypersensitivity:

The management of Type 3 hypersensitivity reactions typically involves controlling inflammation and suppressing the immune response. This may include the use of anti-inflammatory medications, corticosteroids, and immunosuppressive drugs.

Type 3 hypersensitivity reactions can cause significant tissue damage and contribute to the pathogenesis of various autoimmune diseases. Understanding the underlying mechanisms and identifying the specific antigens involved can aid in developing targeted therapies to manage these immune-mediated disorders effectively.

Type 4 hypersensitivity is a delayed-type hypersensitivity reaction that occurs when the immune system mounts a cell-mediated immune response against specific antigens. Unlike Type 1, 2, and 3 hypersensitivity, which involve antibody-mediated mechanisms, Type 4 hypersensitivity is primarily mediated by T cells and does not involve antibodies. This type of hypersensitivity is characterized by a delayed onset, typically occurring 24 to 72 hours after exposure to the antigen. Here's how Type 4 hypersensitivity occurs:

1. Sensitization:

Upon initial exposure to an antigen, antigen-presenting cells (APCs) process the antigen and present its fragments to helper T cells (specifically, CD4+ T cells) in the context of major histocompatibility complex II (MHC II) molecules.

2. Activation of Memory T Cells:

During sensitization, memory T cells specific to the antigen are generated and remain in the body. Upon subsequent exposure to the same antigen, these memory T cells quickly recognize and respond to the antigen.

3. T Cell Activation and Cytokine Release:

The memory T cells recognize the antigen and become activated. They release cytokines, such as interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), which attract and activate other immune cells, such as macrophages and cytotoxic T cells.

4. Recruitment of Effector Cells:

Activated macrophages and cytotoxic T cells target and attack the tissues expressing the antigen. This leads to tissue damage and inflammation at the site of exposure.

Clinical Examples of Type 4 Hypersensitivity:

1. Contact Dermatitis:

Contact dermatitis is a common example of Type 4 hypersensitivity. It occurs when the skin comes into contact with an allergen, such as certain metals, plants (e.g., poison ivy), or chemicals (e.g., certain cosmetics or topical medications). Sensitization occurs during the initial exposure, and subsequent contact with the same allergen triggers a delayed inflammatory response, leading to redness, itching, and skin rash at the site of contact.

2. Tuberculin Skin Test (Mantoux Test):

The tuberculin skin test is used to diagnose exposure to tuberculosis (TB) bacteria. A small amount of TB antigen (purified protein derivative, PPD) is injected into the skin. If an individual has been previously exposed to TB, memory T cells specific to TB antigens will recognize the PPD, leading to a localized skin reaction at the injection site.

3. Allergic Contact Dermatitis:

Similar to contact dermatitis, allergic contact dermatitis occurs when the skin is exposed to an allergen. In this case, the allergen triggers a Type 4 hypersensitivity response, leading to a delayed skin reaction.

Treatment of Type 4 Hypersensitivity:

Treatment of Type 4 hypersensitivity reactions involves managing inflammation and suppressing the immune response. Corticosteroids and immunosuppressive drugs are commonly used to control the inflammatory reaction.

Overall, Type 4 hypersensitivity reactions involve a cell-mediated immune response initiated by T cells. The delayed onset of these reactions sets them apart from the other types of hypersensitivity, making them unique in terms of their underlying mechanisms and clinical manifestations.

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MCQ Test on Hypersensitivity Reactions

MCQ Test on Hypersensitivity Reactions

Q1. Hypersensitivity reactions are classified into:

a) Type A and Type B
b) Immediate and Delayed
c) Type I, Type II, Type III, and Type IV
d) IgG and IgM

Q2. Type I hypersensitivity reactions are mediated by:

a) IgG
b) IgE
c) IgM
d) IgA

Q3. Which type of hypersensitivity reaction involves cytotoxic antibodies?