Module 7: Immune System Pathophysiology

Seasonal allergic rhinitis is most involved in type II hypersensitivity reactions. T/F

False Seasonal allergic rhinitis is most involved in type I hypersensitivity reactions.

Myasthenia gravis is a type II hypersensitivity disorder that involves - impaired muscle function. - symptoms of hyperthyroidism. - symptoms of arthritis or polyarthralgia. - symptoms of glomerular disease.

impaired muscle function. Myasthenia gravis involves muscle weakness caused by loss of acetylcholine stimulation at the motor end-plate. Symptoms of hyperthyroidism occur in Graves disease. Symptoms of arthritis or polyarthralgia occur in systemic lupus erythematosus, a type II hypersensitivity disorder. Glomerular disease can occur in type III hypersensitivity disorders.

When antigen-antibody complexes are formed in the blood, which of the following processes can occur? - Precipitation of the antigen-antibody complex - Phagocytosis of the antigen-antibody complex - Neutralization of the antigen - All of the above

All of the above

What is the major function of T helper cells? - Triggering degranulation of mast cells - Producing antibodies against autoantigens - Killing virus-infected and potentially malignant cells - Secreting cytokines that regulate immune response

Secreting cytokines that regulate immune response

Which disorder is associated with a type III hypersensitivity mechanism of injury? - Systemic lupus erythematosus - Graves disease - Erythroblastosis fetalis - Seasonal allergic rhinitis

Systemic lupus erythematosus Systemic lupus erythematosus is a type III hypersensitivity disorder. Type III hypersensitivity is characterized by antigen-antibody complex deposition into tissues, with consequent activation of complement and a subsequent self-sustaining inflammatory reaction. Graves disease and erythroblastosis fetalis are type II hypersensitivity reactions. Seasonal allergic rhinitis is a type I hypersensitivity reaction.

Anaphylaxis may occur in certain hypersensitivity reactions, including type (Select all that apply.) - I. - II. - III. - IV.

- I. - II.

When mast cells degranulate, they release: - perforins and other toxins. - histamine and other inflammatory mediators. - complement. - antibodies.

histamine and other inflammatory mediators. Mast cells release inflammatory mediators such as histamine when they degranulate.

Which of the following cells are strong phagocytes? - Macrophages - T lymphocytes - Plasma cells - Natural killer cells

Macrophages

Which of the following cells produce antibodies? - T cells - Mast cells - Plasma cells - Macrophages

Plasma cells Plasma cells are mature B lymphocytes that have developed the capacity to produce antibodies during an immune response.

After degranulation, mast cells release prostaglandins and leukotrienes that perform which of the following functions? - Vasodilation and increased vascular permeability - Attract neutrophils and eosinophils - Activate the complement cascade - Opsonization of bacteria

Vasodilation and increased vascular permeability Inflammatory chemicals such as prostaglandins and leukotrienes cause vasodilation and increased vascular permeability.

A naive B cell is a B lymphocyte that: - is dysfunctional and marked for apoptosis. - has not left the thymus. - has not been presented with an antigen. - produces antibodies.

has not been presented with an antigen.

An important mediator of a type I hypersensitivity reaction is - complement. - antigen-antibody immune complexes. - T cells. - histamine.

histamine Histamine mediates type I hypersensitivity reactions. Complement mediates type II hypersensitivity reactions. Antigen-antibody immune complexes mediate type III hypersensitivity reactions. T cells mediate type IV hypersensitivity reactions.

Autoimmune diseases result from (Select all that apply.) - overactive immune function. - increase in self-tolerance. - failure of the immune system to differentiate self and nonself molecules. - communicable infections.

- overactive immune function. - failure of the immune system to differentiate self and nonself molecules. Autoimmunity results from a functional increase in the activity of the immune system. Breakdown of self-tolerance occurs. Genetic and environmental factors are thought to contribute to autoimmunity. Autoimmune disease results from failure of the immune system to differentiate self and nonself molecules; this results in immune reactions that attack normal tissue.

Secondary immune deficiency problems may be caused by (Select all that apply.) - surgery. - high blood sugar. - corticosteroids. - genetic disorders. - low protein level.

- surgery. - high blood sugar. - corticosteroids. - low protein level. Surgery leads to reduced B and T-cell counts. High blood sugar decreases WBC function. Corticosteroids are immunosuppressive. Antibodies are composed of proteins; low protein level impairs antibody synthesis. Genetic abnormalities of immune components lead to primary immune deficiency problems.

What is the function of H1 receptors for histamine on white blood cells? - Activating neutrophils and macrophages - Reducing phagocytosis - Inhibiting degranulation - Increasing vascular permeability

Activating neutrophils and macrophages

How does a cytotoxic T lymphocyte kill another cell? - By secreting cytokines that attract phagocytes - By producing antibodies that opsonize it - By phagocytizing it directly - By secreting perforins and granzymes

By secreting perforins and granzymes Cytotoxic T lymphocytes secrete perforins and granzymes that cause cell death.

In addition to antibodies, which of the following molecules act as opsonins? - Histamine - Complement proteins - Fibrin - Antigens

Complement proteins

Which end of an antibody binds to an antigen? - Fc - Fab - TH1 - TH2

Fab The Fab end of an antibody binds to antigen.

Which disorder is considered a primary immunodeficiency disease? - HIV/AIDS - Malnutrition immunodeficiency - Cancer immunodeficiency - Radiation immunodeficiency

HIV/AIDS HIV/AIDS is a primary immunodeficiency disease involving destruction of T helper cells. Malnutrition immunodeficiency is a secondary immunodeficiency disorder and leads to T-cell destruction and dysfunction. Cancer immunodeficiency is a secondary immunodeficiency disorder caused by the destruction of rapidly proliferating cells from chemotherapeutic agents. Radiation immunodeficiency is a secondary immunodeficiency disorder caused by the destruction of rapidly proliferating cells from the effects of radiation.

Certain autoimmune diseases are associated with the presence of specific proteins on a person's cells. These proteins are called ________ proteins. - complement - antibody receptor - HLA or MHC - TCR or BCR

HLA or MHC Human major histocompatibility complex (MHC) genes located on chromosome 6p21 (also called human leukocyte antigen (HLA) genes) are frequently associated with certain autoimmune disorders. Complement, antibody receptors, and TCR or BCR are not factors in development of autoimmune disease.

A child with a history of recent strep throat infection develops glomerulonephritis. This is most likely a type _____ hypersensitivity reaction. - I. - II. - III. - IV.

III Immune complex glomerulonephritis (an inflammatory renal disorder) is an example of a type III hypersensitivity reaction. The circulating immune complex is then deposited in the glomerular capillary wall and mesangium. Glomerulonephritis secondary to strep throat is not a type I, II, or IV sensitivity reaction.

The hypersensitivity reaction that does not involve antibody production is type - I. - II. - III. - IV.

IV Type IV hypersensitivity reactions do not involve antibody production. The principal mediators are lymphocytes, including T helper cells (Th) that mediate the reaction by releasing lymphokines (cytokines) and/or antigen-sensitized cytotoxic T cells (Tc) that can directly kill cells. The other types involve antibody production. Type I involves IgE; type II involves IgM or IgG; type III involves IgG.

The predominant antibody of a typical allergic response is: - IgG. - IgM. - IgE. - IgA.

IgE (IgA is the predominant antibody in mucosal membrane secretions.)

The principle Ig mediator of type I hypersensitivity reactions is - IgA. - IgG. - IgM. - IgE.

IgE Immunoglobulin E (IgE) is the principal antibody mediating type I hypersensitivity reactions. IgA is not the primary Ig mediator of type I hypersensitivity reactions. IgG is involved in type II hypersensitivity reactions. IgM is involved in type II hypersensitivity reactions.

Severe combined immunodeficiency (SCID) syndrome is an example of a(n) - deficient immune response. - excessive immune response. - primary acquired immunodeficiency. - hypersensitivity reaction.

deficient immune response. SCID syndrome is an example of a deficient immune response in which the immune response is ineffective because of disease-causing genotypes or secondary/acquired dysfunction. An excessive immune response includes disorders in which the immune system is overfunctioning or hyperfunctioning. HIV/AIDS is an example of a primary acquired immunodeficiency disorder. Hypersensitivity reactions are an excessive immune response.

Patients with immunodeficiency disorders are usually first identified because they - run high fevers. - have unusually high WBC counts. - develop brain infections. - develop recurrent infections.

develop recurrent infections The first clinical indicators of immunodeficiency disorders are the signs and symptoms of infection, and the disorders are often first suspected when an individual has severe recurrent, unusual, or unmanageable infections. High fevers can occur in patients who have an intact immune system. Because of the immune deficiency, patients with immunodeficiency disorders may not demonstrate expected WBC counts with infection. Infections in patients with immunodeficiency disorders can occur anywhere in the body.

The effects of histamine release include - vasoconstriction. - bronchodilation. - increased vascular permeability. - decreased gut permeability.

increased vascular permeability. Histamine release leads to increased vascular permeability, which fosters fluid movement out of capillaries and into tissues leading to the edema common in type I hypersensitivity. Histamine leads to bronchoconstriction, increased gut permeability, and vasodilation (not vasoconstriction).

Dramatic hypotension sometimes accompanies type I hypersensitivity reactions, because - massive histamine release from mast cells leads to vasodilation. - toxins released into the blood interfere with cardiac function. - anaphylaxis results in large volume losses secondary to sweating. - hypoxia resulting from bronchoconstriction impairs cardiac function.

massive histamine release from mast cells leads to vasodilation. Hypotension can occur in type I hypersensitivity resulting from massive histamine release leading to vasodilation. Toxins are not released during type I hypersensitivity reactions. Sweating occurs as a reaction to shock from severe hypotension; the hypotension occurs first and is because of histamine release. Hypoxia occurs in anaphylaxis as a result of shock from severe hypotension; the hypotension occurs first and is because of histamine release.

A primary effector cell of the type I hypersensitivity response is - monocytes. - mast cells. - neutrophils. - cytotoxic cells.

mast cells Mast cells are a primary effector cell of the type I hypersensitivity response. Monocytes, neutrophils, and cytotoxic cells are not primary effectors of the type I hypersensitivity response.

The precursor cell to the macrophage is the: - neutrophil. - eosinophil. - plasma cell. - monocyte.

monocyte Monocytes produced by the bone marrow circulate in the blood, from which they enter tissue and mature into macrophages.

RhoGAM (an Rh antibody) would be appropriate in an Rh-_____ woman with an _____ Rh-_____ antibody titer carrying an Rh-_____ fetus. - negative; positive; positive - positive; negative; negative - negative; negative; positive - negative; negative; negative

negative; negative; positive If a woman is Rh-negative, RhoGAM is administered for prevention of Rh-positive antibodies. Erythroblastosis fetalis develops during pregnancy when an Rh-negative mother is sensitized to her fetus's Rh-positive red cell group antigens because of exposure during her current or a previous pregnancy. RhoGAM contains antibodies against Rh antigens on fetal blood cells and is given to the mother to destroy fetal cells that may be present in her circulation before her immune system becomes activated and begins to produce anti-Rh antibodies. RhoGAM is not effective if the mother already has a positive antibody titer for fetal Rh antigens. An Rh-positive woman with negative Rh antibody titer carrying Rh-negative fetus does not require RhoGAM because the mother is Rh-positive and the fetus is Rh-negative.

The process of covering bacteria with antibodies to promote phagocytosis of the microorganisms is called: - neutralization. - precipitation. - margination. - opsonization

opsonization The Fc portions of the antibodies that cover an opsonized microorganism attract phagocytes.

Transfusion reactions involve RBC destruction caused by - donor antigens. - recipient antibodies. - donor T cells. - recipient T cells.

recipient antibodies. The recipient of the blood transfusion has antibodies to the donor's red blood cell (RBC) antigens; the antibodies destroy large numbers of RBC. Donor antigens, donor T, and recipient T cells do not cause transfusion reactions.

The most common primary immune deficiency that affects only B cells is - DiGeorge. - Bruton agammaglobulinemia. - Wiskott-Aldrich. - selective IgA

selective IgA The most common B-cell primary immunodeficiency disorder is selective IgA deficiency. This disorder affects 1:2000 persons. DiGeorge is a T-cell primary immune deficiency. Bruton agammaglobulinemia is not the most common primary immune deficiency affecting B cells; frequency of disease is 1:250,000 males. Females are carriers. Wiskott-Aldrich affects both T cells and B cells.