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WorksheetsChapter 19
Total questions: 22
Worksheet time: 11mins
Type I (Anaphylaxis) hypersensitivity reactions can present as which of the following?
Only systemic reactions such as shock
Only local reactions such as hives
Both local reactions (like hives) and systemic reactions (like anaphylactic shock)
Neither local nor systemic reactions
What is the key mechanism involved in a Type I hypersensitivity reaction?
IgG binding to soluble antigens in the bloodstream
IgM attaching to red blood cells and activating complement
IgE binding to mast cells and basophils after exposure to an antigen
T cells releasing cytokines 48–72 hours after antigen exposure
In Type I hypersensitivity reactions, IgE antibodies bind to which two types of cells?
Neutrophils and macrophages
Mast cells in mucous membranes and basophils in the blood
Dendritic cells and natural killer cells
Eosinophils and platelets
What event occurs when an antigen binds to IgE on mast cells or basophils during a Type I hypersensitivity reaction?
Activation of T cells and delayed cytokine release
Formation of immune complexes that deposit in tissues
Release of chemical mediator granules through degranulation
Activation of complement leading to cell lysis
What is the term for the process in which mast cells and basophils release chemical mediators during a Type I hypersensitivity reaction?
Opsonization
Agglutination
Degranulation
Hemolysis
What is the primary effect of histamine released during a Type I hypersensitivity reaction?
Activation of T cells that cause delayed inflammation
Increased blood vessel permeability, redness, swelling, mucus secretion, and smooth muscle contraction
Formation of immune complexes that deposit in tissues
Complement activation leading to lysis of target cells
Besides histamine, which mediators also contribute to inflammation in Type I hypersensitivity reactions?
Complement proteins and macrophages
Leukotrienes and prostaglandins
Interferons and natural killer cells
IgM and IgG antibodies
What is the primary mechanism of Type II (Cytotoxic) hypersensitivity reactions?
IgE binding to mast cells and triggering degranulation
IgG or IgM binding to soluble antigens forming immune complexes
IgG or IgM binding to cell-bound antigens and activating complement, leading to cell lysis
T cell–mediated cytokine release after a delayed response
In a drug-induced cytotoxic reaction, such as thrombocytopenic purpura, how does the drug trigger an immune response?
The drug directly destroys platelets without involving the immune system
The drug acts as a hapten, coating platelets and making them appear foreign to the immune system
The drug forms soluble immune complexes that deposit in tissues
The drug activates T cells to release cytokines after 1–2 days
What occurs in drug-induced agranulocytosis?
Destruction of red blood cells due to complement activation
Destruction of granulocytic white blood cells caused by a drug
Formation of immune complexes that deposit in the kidneys
Activation of mast cells and release of histamine
What happens in hemolytic anemia as a type of Type II hypersensitivity reaction?
Destruction of granulocytic white blood cells
Destruction of red blood cells by antibodies and complement
Formation of immune complexes in the bloodstream
Delayed T cell–mediated inflammation
What characterizes Type III (Immune Complex) hypersensitivity reactions?
IgE antibodies bind to mast cells and basophils
IgG or IgM antibodies bind to cell-surface antigens, causing cell lysis
Antibodies, usually IgG, bind to soluble antigens in the serum, forming immune complexes
T cells mediate a delayed response causing tissue inflammation
What is the result of immune complex deposition in Type III hypersensitivity reactions?
Degranulation of mast cells and histamine release
Destruction of red blood cells by complement
Inflammation and tissue damage, such as glomerulonephritis in the kidneys
Which of the following best describes Type IV (Delayed Cell-Mediated) hypersensitivity reactions?
Immediate reaction mediated by IgE and mast cells
Antibody-mediated lysis of red or white blood cells
Formation of immune complexes that deposit in tissues
T cell–mediated response that occurs a day or more after antigen exposure
Why are Type IV hypersensitivity reactions delayed?
Because IgE antibodies take time to bind to mast cells
Because complement proteins must slowly accumulate in tissues
Because T cells and macrophages need time to migrate and accumulate near the foreign antigen
Because antibodies form immune complexes before causing inflammation
Which of the following are examples of Type IV (Delayed Cell-Mediated) hypersensitivity reactions?
Hives and anaphylactic shock
Hemolytic anemia and thrombocytopenic purpura
Contact dermatitis and the TB skin test
Glomerulonephritis and serum sickness
In Type IV hypersensitivity reactions, what happens after macrophages phagocytize an antigen?
The antigen is immediately destroyed without affecting T cells
The antigen is presented to T cell receptors, causing proliferation of T cells and memory cells
Antibodies bind to the antigen and trigger complement activation
Mast cells release histamine and other chemical mediators
During a Type IV hypersensitivity reaction, what occurs upon re-exposure to the antigen?
IgE antibodies bind to mast cells and trigger degranulation
Complement proteins lyse target cells immediately
Memory T cells activate T cells, which release cytokines and cause inflammation
Soluble antigen-antibody complexes form and deposit in tissues
Why does a TB skin test cause a reaction within 1–2 days in someone previously exposed to Mycobacterium tuberculosis?
Because IgE antibodies trigger mast cell degranulation
Because complement lyses infected cells immediately
Because memory T cells recognize the antigen, activating T cells and causing a delayed inflammatory response
Because immune complexes deposit in the skin
What is immunodeficiency?
Overactivation of the immune system causing allergies
Lack of a functioning immune system or missing immune components
Formation of immune complexes in tissues
Delayed T cell–mediated inflammation
What characterizes a primary (congenital) immunodeficiency?
It develops later in life due to infections or drugs
It is caused by overproduction of antibodies
It is present at birth and usually results from genetic defects
It only affects T cells temporarily
Which of the following is an example of a secondary (acquired) immunodeficiency?
Severe Combined Immunodeficiency (SCID) present at birth
HIV infection leading to AIDS
Congenital absence of B cells
Genetic defect in complement proteins
