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1. Which of the following are considered the "first responders" of the innate
immune system?: Neutrophils; they appear first in any immune response
2. Hives (urticaria) are an example of a:
a. Type 1 Hypersensitivity reaction
b. Type 2 Hypersensitivity reaction
c. Type 3 Hypersensitivity reaction
d. Type 4 Hypersensitivity reaction: A. Type 1 hypersensitivity reaction; hives
(urticarial) are an example of a Type 1 hypersensitivity reaction mediated by the
antibody, IgE and mast cells
3. Anaphylaxis is a hypersensitivity reaction
a. Type 1
b. Type 2
c. Type 3
d. Type 4: A. Type 1; they are mediated by IgE and mast cells. An individual who is
highly sensitized to the antigen may experience anaphylaxis
4. Allergic contact dermatitis is an example of hypersensitivity reac-
tion.
a. Type 1
b. Type 2
c. Type 3
d. Type 4: D. Allergic contact dermatitis is an example of Type 4 hypersensitivity
reaction mediated by T-cells. When the individual comes in contact with the allergen
(ex. poison ivy), an antigen complex is formed. On subsequent exposure to the
antigen, sensitized T-cells activate the inflammatory process that causes the allergic
contact dermatitis to appear
5. Type 2 (Cytotoxic) Hypersensitivity reactions are mediated by:
a. IgA or IgE
b. IgM or IgA
c. IgG or IgM
d. IgE or IgG: C. Type 2 hypersensitivity reaction is mediated by IgG or IgM
6. Type 1: Allergic Reaction: On initial encounter with an allergen, the individual
will first produce IgE antibodies. After the allergen is cleared, the remaining IgE
molecules will be bound by mast cells, basophils, and eosinophils that contain
receptors for the IgE molecules. This process is referred to as sensitization. On
subsequent exposure to the allergen, the IgE molecules located on the sensitized
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cells induces their immediate degranulation. This causes the release of inflamma-
tory mediators such as histamine, leukotrienes, and prostaglandins that results in
vasodilation, bronchial smooth muscle contraction, and mucus production. Type I
hypersensitivity reactions can be local or systemic. Systemic reactions can result in
anaphylaxis, a potentially life-threatening condition. Allergic asthma is an example
of a Type I hypersensitivity reaction. On exposure to certain allergens (typically
inhaled), individuals with allergic asthma experience inflammation of the airways,
characterized by tissue swelling and excessive mucus production. This narrowing of
the airways makes it difficult to breathe.
7. Type 2: Tissue-Specific: A Type II hypersensitivity reaction is tissue-specific and
usually occurs as a result of haptens that cause an IgG antibody or IgM antibody
mediated response. The antibodies are specifically directed to the antigen located
on the cell membrane. A hapten is a small molecule that can cause an immune
response when it attaches to a protein. Macrophages are the primary effector cells
of Type II responses. Typical examples of Type II reactions are drug allergies, as well
as allergies against infectious agents. The Type II response begins with the antibody
binding to the antigen and may cause the following:
1. The cell to be destroyed by the antibody
2. Cell destruction through phagocytosis by macrophages
3. Damage to the cell by neutrophils triggering phagocytosis
4. Natural killer cells to release toxic substances that destroy the target cell
5. Malfunction of the cell without destruction
Examples of type II reactions include drug allergies, hemolytic anemia, blood trans-
fusion mismatch with resulting transfusion reaction and Rh hemolytic disease.
8. Type 3: Immune-Complex Reaction: The Type III hypersensitivity reaction is
also an antigen-antibody response. The major difference between Type II and Type III
responses is that in a Type II response, the antibody binds to the antigen on the cell
surface, but in Type III responses, the antibody binds to the antigen in the blood or
body fluids and then circulates to the tissue. Type III reactions are not organ specific
and use neutrophils as the primary effector cell. In type III hypersensitivity reactions
immune-complex deposition (ICD) causes autoimmune diseases, which is often a
complication. As the disease progresses a more accumulation of immune-complex-
es occurs, and when the body becomes overloaded the complexes are deposited in
the tissues and cause inflammation as the mononuclear phagocytes, erythrocytes,
and complement system fail to remove immune complexes from the blood. One of
the classic Type III reactions is serum sickness.
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9. Type 4: Cell-Mediated/Delayed Reaction: The type IV hypersensitivity reactions
are known as cell-mediated responses and use lymphocytes and macrophages as
primary mediators. Unlike the first three types of responses, which are humoral
immune functions, a Type IV response is mediated by T-lymphocytes and does not
use antibodies. A typical reaction from a Type IV cell-mediated response would be a
localized contact dermatitis. When the individual comes in contact with the antigen,
T-cells are activated and move to the area of the antigen. The antigen is taken up,
processed, and presented to macrophages, leading to epidermal reactions charac-
terized by erythema, cellular infiltration and vesicles. This process is illustrated in
contact dermatitis.
10. Type 1 Hypersensitivity Summary: Mechanism: IgE action on mast cells
Examples: Hay fever
Pathology: Mast cell degranulation results in an inflammatory response
11. Type 2 Hypersensitivity Summary: Mechanism: Tissue-specific destruction or
impairment because of:
1. Antibody binding followed by lysis via complement
2. Antibody binding followed by macrophage phagocytosis
3. Antibody binding followed by neutrophil destruction
4. Antibody-dependent cell (NK)-mediated cytotoxicity, or
5. Antireceptor antibodies
Examples: 1-ABO incompatibility
5-Graves' disease
Pathology: 1-Complement damages RBC membrane and cells lyse
5-Autoantibodies specific for thyroid tissue impair receptor for TSH
12. Type 3 Hypersensitivity Summary: Mechanism: Antigen-Antibody complex
deposited in tissues
Examples: Raynaud's phenomenon
Pathology: Complex deposited in small peripheral vessels in cool temperatures
leading to vasoconstriction and blocked circulation
13. Type 4 cytotoxic hypersensitivity reactions are mediated by:
a. B-cells
b. T-cells
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c. IgA
d. IgM: B. Type 4 hypersensitivity reaction is mediated by T-cells
14. The diagnosis for an individual who presents to the office with sudden
swollen lips and eyes, shortness of breath and throat tightness after a bee
sting is:
a. anaphylaxis
b. asthma
c. reactive airway disease
d. angioedema: A. Anaphylaxis; the symptoms are consistent with the life=threat-
ening condition, anaphylaxis after being exposed to a bee sting
15. Damage occurs with ABO incompatibility because:
a. Antigen/Antibody complexes attack the RBC
b. Complement damages RBC membrane causing cell lysis
c. Autoantibodies specific for thyroid tissue impairs the receptors for TSH
d. Mast cell degranulation: B. Complement damages RBC membrane causing cell
lysis
16. Which of the following is the underlying pathology for hay fever?
a. Formation of autoantibodies
b. Destruction by T-cells
c. Mast cell degranulation
d. Activation of complement: C. Mast cell degranulation; hay fever falls under a
type 1 hypersensitivity reaction where mast cell degranulation is the underlying
pathology that produces the symptoms
17. An example of primary immunodeficiency is:
a. Chronic Granulomatous Disease
b. Sinus Infection
c. Pneumonia
d. Human Immunodeficiency Virus: A. Chronic granulomatous disease (CGD) is
an example of a primary immunodeficiency
18. An example of a secondary immunodeficiency is:
a. Pneumocystis Carinii
b. Common Variable Immunodeficiency
c. Job Syndrome
d. Familial Mediterranean Fever: A. Pneumocystis Carinii is an example of a
Questions with Correct Answers | Guaranteed PassS
1. Which of the following are considered the "first responders" of the innate
immune system?: Neutrophils; they appear first in any immune response
2. Hives (urticaria) are an example of a:
a. Type 1 Hypersensitivity reaction
b. Type 2 Hypersensitivity reaction
c. Type 3 Hypersensitivity reaction
d. Type 4 Hypersensitivity reaction: A. Type 1 hypersensitivity reaction; hives
(urticarial) are an example of a Type 1 hypersensitivity reaction mediated by the
antibody, IgE and mast cells
3. Anaphylaxis is a hypersensitivity reaction
a. Type 1
b. Type 2
c. Type 3
d. Type 4: A. Type 1; they are mediated by IgE and mast cells. An individual who is
highly sensitized to the antigen may experience anaphylaxis
4. Allergic contact dermatitis is an example of hypersensitivity reac-
tion.
a. Type 1
b. Type 2
c. Type 3
d. Type 4: D. Allergic contact dermatitis is an example of Type 4 hypersensitivity
reaction mediated by T-cells. When the individual comes in contact with the allergen
(ex. poison ivy), an antigen complex is formed. On subsequent exposure to the
antigen, sensitized T-cells activate the inflammatory process that causes the allergic
contact dermatitis to appear
5. Type 2 (Cytotoxic) Hypersensitivity reactions are mediated by:
a. IgA or IgE
b. IgM or IgA
c. IgG or IgM
d. IgE or IgG: C. Type 2 hypersensitivity reaction is mediated by IgG or IgM
6. Type 1: Allergic Reaction: On initial encounter with an allergen, the individual
will first produce IgE antibodies. After the allergen is cleared, the remaining IgE
molecules will be bound by mast cells, basophils, and eosinophils that contain
receptors for the IgE molecules. This process is referred to as sensitization. On
subsequent exposure to the allergen, the IgE molecules located on the sensitized
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cells induces their immediate degranulation. This causes the release of inflamma-
tory mediators such as histamine, leukotrienes, and prostaglandins that results in
vasodilation, bronchial smooth muscle contraction, and mucus production. Type I
hypersensitivity reactions can be local or systemic. Systemic reactions can result in
anaphylaxis, a potentially life-threatening condition. Allergic asthma is an example
of a Type I hypersensitivity reaction. On exposure to certain allergens (typically
inhaled), individuals with allergic asthma experience inflammation of the airways,
characterized by tissue swelling and excessive mucus production. This narrowing of
the airways makes it difficult to breathe.
7. Type 2: Tissue-Specific: A Type II hypersensitivity reaction is tissue-specific and
usually occurs as a result of haptens that cause an IgG antibody or IgM antibody
mediated response. The antibodies are specifically directed to the antigen located
on the cell membrane. A hapten is a small molecule that can cause an immune
response when it attaches to a protein. Macrophages are the primary effector cells
of Type II responses. Typical examples of Type II reactions are drug allergies, as well
as allergies against infectious agents. The Type II response begins with the antibody
binding to the antigen and may cause the following:
1. The cell to be destroyed by the antibody
2. Cell destruction through phagocytosis by macrophages
3. Damage to the cell by neutrophils triggering phagocytosis
4. Natural killer cells to release toxic substances that destroy the target cell
5. Malfunction of the cell without destruction
Examples of type II reactions include drug allergies, hemolytic anemia, blood trans-
fusion mismatch with resulting transfusion reaction and Rh hemolytic disease.
8. Type 3: Immune-Complex Reaction: The Type III hypersensitivity reaction is
also an antigen-antibody response. The major difference between Type II and Type III
responses is that in a Type II response, the antibody binds to the antigen on the cell
surface, but in Type III responses, the antibody binds to the antigen in the blood or
body fluids and then circulates to the tissue. Type III reactions are not organ specific
and use neutrophils as the primary effector cell. In type III hypersensitivity reactions
immune-complex deposition (ICD) causes autoimmune diseases, which is often a
complication. As the disease progresses a more accumulation of immune-complex-
es occurs, and when the body becomes overloaded the complexes are deposited in
the tissues and cause inflammation as the mononuclear phagocytes, erythrocytes,
and complement system fail to remove immune complexes from the blood. One of
the classic Type III reactions is serum sickness.
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9. Type 4: Cell-Mediated/Delayed Reaction: The type IV hypersensitivity reactions
are known as cell-mediated responses and use lymphocytes and macrophages as
primary mediators. Unlike the first three types of responses, which are humoral
immune functions, a Type IV response is mediated by T-lymphocytes and does not
use antibodies. A typical reaction from a Type IV cell-mediated response would be a
localized contact dermatitis. When the individual comes in contact with the antigen,
T-cells are activated and move to the area of the antigen. The antigen is taken up,
processed, and presented to macrophages, leading to epidermal reactions charac-
terized by erythema, cellular infiltration and vesicles. This process is illustrated in
contact dermatitis.
10. Type 1 Hypersensitivity Summary: Mechanism: IgE action on mast cells
Examples: Hay fever
Pathology: Mast cell degranulation results in an inflammatory response
11. Type 2 Hypersensitivity Summary: Mechanism: Tissue-specific destruction or
impairment because of:
1. Antibody binding followed by lysis via complement
2. Antibody binding followed by macrophage phagocytosis
3. Antibody binding followed by neutrophil destruction
4. Antibody-dependent cell (NK)-mediated cytotoxicity, or
5. Antireceptor antibodies
Examples: 1-ABO incompatibility
5-Graves' disease
Pathology: 1-Complement damages RBC membrane and cells lyse
5-Autoantibodies specific for thyroid tissue impair receptor for TSH
12. Type 3 Hypersensitivity Summary: Mechanism: Antigen-Antibody complex
deposited in tissues
Examples: Raynaud's phenomenon
Pathology: Complex deposited in small peripheral vessels in cool temperatures
leading to vasoconstriction and blocked circulation
13. Type 4 cytotoxic hypersensitivity reactions are mediated by:
a. B-cells
b. T-cells
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c. IgA
d. IgM: B. Type 4 hypersensitivity reaction is mediated by T-cells
14. The diagnosis for an individual who presents to the office with sudden
swollen lips and eyes, shortness of breath and throat tightness after a bee
sting is:
a. anaphylaxis
b. asthma
c. reactive airway disease
d. angioedema: A. Anaphylaxis; the symptoms are consistent with the life=threat-
ening condition, anaphylaxis after being exposed to a bee sting
15. Damage occurs with ABO incompatibility because:
a. Antigen/Antibody complexes attack the RBC
b. Complement damages RBC membrane causing cell lysis
c. Autoantibodies specific for thyroid tissue impairs the receptors for TSH
d. Mast cell degranulation: B. Complement damages RBC membrane causing cell
lysis
16. Which of the following is the underlying pathology for hay fever?
a. Formation of autoantibodies
b. Destruction by T-cells
c. Mast cell degranulation
d. Activation of complement: C. Mast cell degranulation; hay fever falls under a
type 1 hypersensitivity reaction where mast cell degranulation is the underlying
pathology that produces the symptoms
17. An example of primary immunodeficiency is:
a. Chronic Granulomatous Disease
b. Sinus Infection
c. Pneumonia
d. Human Immunodeficiency Virus: A. Chronic granulomatous disease (CGD) is
an example of a primary immunodeficiency
18. An example of a secondary immunodeficiency is:
a. Pneumocystis Carinii
b. Common Variable Immunodeficiency
c. Job Syndrome
d. Familial Mediterranean Fever: A. Pneumocystis Carinii is an example of a
