Why Am I So Hypersensitive? Take This Immune Reaction Quiz

The correct answer is IgE antibody. When a child is stung by a bee, the body may produce IgE antibodies in response to the bee venom. These antibodies bind to mast cells and basophils, triggering the release of inflammatory mediators such as histamine. This can cause respiratory distress and unconsciousness. IgE antibodies are known to play a crucial role in allergic reactions, including those caused by insect stings.

The child's symptoms of respiratory failure and vascular collapse within minutes after being stung repeatedly by wasps suggest a severe and immediate allergic reaction, known as systemic anaphylaxis. Systemic anaphylaxis occurs when the immune system overreacts to an allergen, such as the wasp venom, causing widespread release of histamine and other chemicals that lead to respiratory distress and low blood pressure. This is the most likely explanation for the child's symptoms in this scenario.

A delayed hypersensitivity reaction is characterized by an infiltrate composed of helper T cells and macrophages. This type of reaction occurs several hours to days after exposure to an antigen and involves the activation of T cells. Helper T cells release cytokines that attract macrophages to the site of inflammation. Macrophages then phagocytose the antigen and release additional inflammatory mediators, leading to tissue damage. This type of reaction is commonly seen in conditions such as contact dermatitis and tuberculin skin testing.

Type II hypersensitivity occurs when antibodies bind to antigens on the surface of cells, leading to cell destruction. In contrast, type III hypersensitivity occurs when antibodies form immune complexes with soluble antigens before they interact with cells. The difference lies in the location of the antibody-antigen interaction. Type II hypersensitivity involves direct binding to cell surface antigens, while type III hypersensitivity involves the formation of immune complexes in the bloodstream. The participation of complement and T cells can occur in both type II and type III hypersensitivity reactions, but it is not the defining difference between the two types.

The lepromin skin test is intended to detect a Type IV hypersensitivity reaction. Type IV hypersensitivity, also known as delayed-type hypersensitivity, is characterized by the activation of T cells and the release of cytokines, resulting in inflammation at the site of antigen exposure. In the case of the lepromin skin test, the injection of inactivated Mycobacterium leprae organisms triggers a delayed hypersensitivity reaction in individuals with leprosy, leading to the development of induration and erythema at the injection site.

Leukotrienes are lipid mediators that play a key role in the inflammatory response, particularly in asthma. In severe asthma, the airways become inflamed and constricted, leading to symptoms such as wheezing, shortness of breath, and coughing. Antihistamines primarily target histamine, which is involved in allergic reactions, but they do not effectively reduce the inflammation caused by leukotrienes. Therefore, if a patient with severe asthma does not experience relief from antihistamines, it is likely because their symptoms are primarily caused by leukotrienes.

The patient's symptoms of fever, rash, and proteinuria suggest an immunologic reaction. IgG and complement are most likely to be involved in this reaction. IgG is an antibody that is produced in response to an infection or inflammation, and complement is a group of proteins that helps to activate the immune response. Together, IgG and complement can cause inflammation and tissue damage, leading to the symptoms seen in the patient.

In anaphylactic hypersensitivity, IgE antibodies are involved in the immune response, leading to the release of inflammatory mediators such as histamine. This type of hypersensitivity is characterized by a rapid and severe allergic reaction. On the other hand, immune complex hypersensitivity involves the formation of antigen-antibody complexes that deposit in tissues, leading to inflammation and tissue damage. Complement proteins are involved in the activation of the immune response in both types of hypersensitivity. However, the statement that less antigen is typically needed to trigger an anaphylactic reaction than an immune complex reaction is the most accurate. Anaphylactic reactions can occur with minimal exposure to allergens, while immune complex reactions generally require a higher antigen load.

Hypersensitivity to penicillin and hypersensitivity to poison oak are both initiated by haptens. Haptens are small molecules that can bind to larger molecules in the body, forming a complex that triggers an immune response. In the case of penicillin, the hapten is the penicillin molecule itself, which can bind to proteins in the body and cause an allergic reaction. Similarly, in the case of poison oak, the hapten is a chemical called urushiol, which is found in the plant and can bind to proteins in the skin, leading to an allergic reaction.

The patient's symptoms, including hypotension, cardiac arrhythmia, bronchoconstriction, and laryngeal edema, indicate a systemic allergic reaction known as anaphylactoid response. The development of IgG antibodies to the anesthetic gas suggests an immune-mediated response. Type III hypersensitivity is characterized by the formation of immune complexes that deposit in tissues, leading to inflammation and tissue damage. This aligns with the patient's severe brain damage due to hypoxernia. Therefore, the correct answer is Type III Hypersensitivity.

Type III hypersensitivity reactions occur when immune complexes form in the bloodstream and deposit in various tissues, leading to inflammation and tissue damage. Symptoms typically occur days to weeks after exposure to the antigen. In this case, the symptoms of chills, fever, and rash developing 8 days after receiving the penicillin injection suggest a delayed immune reaction, which is characteristic of a type III hypersensitivity reaction.

In Henoch-Schonlein purpura, the purpuric rash is caused by IgA immune complexes that induce vasculitis. Henoch-Schonlein purpura is a type of vasculitis characterized by inflammation of the blood vessels. In this condition, IgA immune complexes deposit in the blood vessel walls, leading to an inflammatory response and damage to the vessels. This results in the development of a purpuric rash, which is characterized by small purple spots on the skin caused by bleeding under the skin.