NUR 631 FINAL 1
1. Some older adults have impaired inflammation and wound healing because of which
problem?
Circulatory system cannot adequately perfuse tissues.
Complement and chemotaxis aredeficient.
Underlying chronic illness(es) exists.
Number of mast cells is insufficient.
Answer
C
In some cases, impaired healing is not directly associated with aging, in general, but can instead be
linked to a chronic illness such as cardiovascular disease or diabetes mellitus. Older adults may
have circulatory problems, but that would not lead directly to impaired inflammation and wound
healing. Older people do not have deficient complement and chemotaxis, nor do they have
insufficient mast cell numbers.
2. In which structure does B lymphocytes mature and undergo changes that commit them to
becoming B cells?
Thymus gland
Regional lymph nodes
Bone marrow
Spleen
Answer
C
B lymphocytes mature and become B cells in specialized (primary) lymphoid organs—the
thymus gland for T cells and the bone marrow for B cells. Neither regional lymph nodes nor the
spleen are involved in changing B lymphocytes into B cells.
3. An individual's acquired immunity is dependent on the function of which cells? (Select all
that apply.)
T lymphocytes
B lymphocytes
,Macrophages
Opsonins
Neutrophils
Answer
A, B, C
T lymphocytes, B lymphocytes, macrophages, and dendritic cells are involved in acquired
immunity. Opsonins are molecules that tag microorganisms for destruction by cells of the
inflammatory system; these cells are primarily neutrophils. Neutrophils are white blood cells.
4. The common hay fever allergy is expressed through a reaction that is mediated by which
class of immunoglobulins?
IgE
IgG
IgM
T cells
Answer
A
Type I reactions are mediated by antigen-specific IgE and the products of tissue mast cells. The
most common allergies (e.g., pollen allergies) are type I reactions. In addition, most type I
reactions occur against environmental antigens and are therefore allergic. Hay fever allergy is
not mediated by IgG, IgM, or T cells.
5. During an IgE-mediated hypersensitivity reaction, which leukocyte is activated?
a. Neutrophils
b. Monocytes
c. Eosinophils
d. T lymphocytes
Answer
C
Of the options provided, only eosinophils are activated during IgE-mediated hyper- sensitivity
reactions.
6. During an IgE-mediated hypersensitivity reaction, what causes bronchospasm?
a. Bronchial edema caused by the chemotactic factor of anaphylaxis
,b. Bronchial edema caused by binding of the cytotropic antibody
c. Smooth muscle contraction caused by histamine bound to H1 receptors
d. Smooth muscle contraction caused by histamine bound to H2 receptors
Answer
-
C
During an IgE-mediated hypersensitivity reaction, smooth muscle contraction caused by
histamine bound to H1 receptors results in bronchospasms. The bronchospasm is not caused by
edema or by histamine binding to H2 receptors.
7. A patient is having an IgE-mediated hypersensitivity reaction. What action by the healthcare
professional is best?
a. Give the patient an antihistamine.
b. Prepare to give the patient a blood transfusion.
c. Ask the patient is he/she is having pain at the site.
d. Apply warm, moist heat to the affected area.
Answer
A
Histamine is the most potent mediator in an IgE-mediated hypersensitivity reaction (Type 1).
Histamine bound to H2 results in the degranulation of mast cells with the release of histamine.
Blocking histamine receptors with antihistamines can control some type I responses. The
healthcare professional would not need to give the patient blood; warm; moist heat; or ask
about pain.
8. A student asks about the mechanism that results in type II hypersensitivity reactions. What
description by the professor is best?
a. Antibodies coat mast cells by binding to receptors that signal its degranulation,
followed by a discharge of preformed mediators.
b. Antibodies bind to soluble antigens that were released into body fluids, and
the immune complexes are then deposited in the tissues.
c. Cytotoxic T lymphocytes or lymphokine-producing helper T 1 cells directly attack
and destroy cellular targets.
d. Antibodies bind to the antigens on the cell surface.
Answer
D
The mechanism that results in a type II hypersensitivity reaction begins with antibody binding to
tissue-specific antigens or antigens that have attached to particular tissues. The cell can be
, destroyed by antibody IgG or IgM and activation of the complement cascade through the
classical pathway.
9. How are target cells destroyed in a type II hypersensitivity reaction?
a. Tissue damage from mast cell degranulation
b. Antigen-antibody complexes deposited in vessel walls
c. Cytotoxic T lymphocytes attack the cell directly.
d. Natural killer cells
Answer
D
The mechanism that results in a type II hypersensitivity reaction involves a subpopulation of
cytotoxic cells that are not antigen specific (natural killer [NK] cells). Antibody on the target cell is
recognized by Fc receptors on the NK cells, which releases toxic substances that destroy the target
cell. Tissue damage from mast cell degranulation occurs in type I hypersensitivity reactions.
Antigen-antibody complexes are active in type III hypersensitivity responses. Cytotoxic
lymphocytes are involved in type IV hypersensitivity responses.
10. Graves disease (hyperthyroidism) is an example of which type II hypersensitivity reaction?
a. Modulation
b. Antibody-dependent cell-mediated cytotoxicity
c. Neutrophil-mediated damage
d. Complement-mediated lysis
Answer
A
The antibody reacts with the receptors on the target cell surface and modulates the function of
the receptor by preventing interactions with their normal ligands, replacing the ligand and
inappropriately stimulating the receptor or destroying the receptor. For example, in the
hyperthyroidism (excessive thyroid activity) of Graves disease, autoantibody binds to and
activates receptors for thyroid-stimulating hormone (TSH) (a pituitary hormone that controlsthe
production of the hormone thyroxine by the thyroid). Graves disease is not a result of cell-
mediated cytotoxicity, neutrophil-mediated damage, or complement-mediated lysis.
11. Immunoglobulin E (IgE) is associated with which type of hypersensitivity reaction?
a. I
b. II c. III d. IV
Answer
A
1. Some older adults have impaired inflammation and wound healing because of which
problem?
Circulatory system cannot adequately perfuse tissues.
Complement and chemotaxis aredeficient.
Underlying chronic illness(es) exists.
Number of mast cells is insufficient.
Answer
C
In some cases, impaired healing is not directly associated with aging, in general, but can instead be
linked to a chronic illness such as cardiovascular disease or diabetes mellitus. Older adults may
have circulatory problems, but that would not lead directly to impaired inflammation and wound
healing. Older people do not have deficient complement and chemotaxis, nor do they have
insufficient mast cell numbers.
2. In which structure does B lymphocytes mature and undergo changes that commit them to
becoming B cells?
Thymus gland
Regional lymph nodes
Bone marrow
Spleen
Answer
C
B lymphocytes mature and become B cells in specialized (primary) lymphoid organs—the
thymus gland for T cells and the bone marrow for B cells. Neither regional lymph nodes nor the
spleen are involved in changing B lymphocytes into B cells.
3. An individual's acquired immunity is dependent on the function of which cells? (Select all
that apply.)
T lymphocytes
B lymphocytes
,Macrophages
Opsonins
Neutrophils
Answer
A, B, C
T lymphocytes, B lymphocytes, macrophages, and dendritic cells are involved in acquired
immunity. Opsonins are molecules that tag microorganisms for destruction by cells of the
inflammatory system; these cells are primarily neutrophils. Neutrophils are white blood cells.
4. The common hay fever allergy is expressed through a reaction that is mediated by which
class of immunoglobulins?
IgE
IgG
IgM
T cells
Answer
A
Type I reactions are mediated by antigen-specific IgE and the products of tissue mast cells. The
most common allergies (e.g., pollen allergies) are type I reactions. In addition, most type I
reactions occur against environmental antigens and are therefore allergic. Hay fever allergy is
not mediated by IgG, IgM, or T cells.
5. During an IgE-mediated hypersensitivity reaction, which leukocyte is activated?
a. Neutrophils
b. Monocytes
c. Eosinophils
d. T lymphocytes
Answer
C
Of the options provided, only eosinophils are activated during IgE-mediated hyper- sensitivity
reactions.
6. During an IgE-mediated hypersensitivity reaction, what causes bronchospasm?
a. Bronchial edema caused by the chemotactic factor of anaphylaxis
,b. Bronchial edema caused by binding of the cytotropic antibody
c. Smooth muscle contraction caused by histamine bound to H1 receptors
d. Smooth muscle contraction caused by histamine bound to H2 receptors
Answer
-
C
During an IgE-mediated hypersensitivity reaction, smooth muscle contraction caused by
histamine bound to H1 receptors results in bronchospasms. The bronchospasm is not caused by
edema or by histamine binding to H2 receptors.
7. A patient is having an IgE-mediated hypersensitivity reaction. What action by the healthcare
professional is best?
a. Give the patient an antihistamine.
b. Prepare to give the patient a blood transfusion.
c. Ask the patient is he/she is having pain at the site.
d. Apply warm, moist heat to the affected area.
Answer
A
Histamine is the most potent mediator in an IgE-mediated hypersensitivity reaction (Type 1).
Histamine bound to H2 results in the degranulation of mast cells with the release of histamine.
Blocking histamine receptors with antihistamines can control some type I responses. The
healthcare professional would not need to give the patient blood; warm; moist heat; or ask
about pain.
8. A student asks about the mechanism that results in type II hypersensitivity reactions. What
description by the professor is best?
a. Antibodies coat mast cells by binding to receptors that signal its degranulation,
followed by a discharge of preformed mediators.
b. Antibodies bind to soluble antigens that were released into body fluids, and
the immune complexes are then deposited in the tissues.
c. Cytotoxic T lymphocytes or lymphokine-producing helper T 1 cells directly attack
and destroy cellular targets.
d. Antibodies bind to the antigens on the cell surface.
Answer
D
The mechanism that results in a type II hypersensitivity reaction begins with antibody binding to
tissue-specific antigens or antigens that have attached to particular tissues. The cell can be
, destroyed by antibody IgG or IgM and activation of the complement cascade through the
classical pathway.
9. How are target cells destroyed in a type II hypersensitivity reaction?
a. Tissue damage from mast cell degranulation
b. Antigen-antibody complexes deposited in vessel walls
c. Cytotoxic T lymphocytes attack the cell directly.
d. Natural killer cells
Answer
D
The mechanism that results in a type II hypersensitivity reaction involves a subpopulation of
cytotoxic cells that are not antigen specific (natural killer [NK] cells). Antibody on the target cell is
recognized by Fc receptors on the NK cells, which releases toxic substances that destroy the target
cell. Tissue damage from mast cell degranulation occurs in type I hypersensitivity reactions.
Antigen-antibody complexes are active in type III hypersensitivity responses. Cytotoxic
lymphocytes are involved in type IV hypersensitivity responses.
10. Graves disease (hyperthyroidism) is an example of which type II hypersensitivity reaction?
a. Modulation
b. Antibody-dependent cell-mediated cytotoxicity
c. Neutrophil-mediated damage
d. Complement-mediated lysis
Answer
A
The antibody reacts with the receptors on the target cell surface and modulates the function of
the receptor by preventing interactions with their normal ligands, replacing the ligand and
inappropriately stimulating the receptor or destroying the receptor. For example, in the
hyperthyroidism (excessive thyroid activity) of Graves disease, autoantibody binds to and
activates receptors for thyroid-stimulating hormone (TSH) (a pituitary hormone that controlsthe
production of the hormone thyroxine by the thyroid). Graves disease is not a result of cell-
mediated cytotoxicity, neutrophil-mediated damage, or complement-mediated lysis.
11. Immunoglobulin E (IgE) is associated with which type of hypersensitivity reaction?
a. I
b. II c. III d. IV
Answer
A
