CHAMB ERLAIN NR507 EDAPTS W EEK 1 EDAPT
MODULE QUESTIONS W ITH EX PERT
SOLUTIONS + RATIONALES
❖ Hives (Urticaria) - Type 1 Allergic Reaction – dermal/skin manifestation.
❖ Allergic Contact Dermatitis – Type 4 Allergic Reaction - an example of a Type IV
hypersensitivity reaction mediated by T-cells. When the individual comes in contact with
the antigen (e.g. 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.
❖ Type 2 (Cytotoxic/tissue-specific) hypersensitivity reactions are mediated by: IgG or IgM.
❖ Which of the following are considered the “first responders” of the innate immune
system? Neutrophils appear first in any immune response.
❖ Anaphylaxis is a Type 1 Allergic Reaction - Type 1 hypersensitivity reactions are
mediated by IgE and mast cells. An individual who is highly sensitized to the antigen may
experience anaphylaxis.
❖ Damage occurs with ABO incompatibility because: Complement damages RBC
membrane causing cell lysis. Damage from ABO incompatibility occurs because of the
effects of complement on the RBC membrane that results in RBC lysis.
❖ 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: anaphylaxis. The
symptoms are consistent with the life-threating condition, anaphylaxis after being
exposed. to a bee sting.
❖ Which of the following assessment findings would be expected in a patient who
presents with urticaria? Eosinophilia. Eosinophils are present in the allergic reaction.
❖ Type IV cytotoxic hypersensitivity reactions are mediated by: T-cells.
❖
Types of Hypersensitivity Reactions
Type ❖ Mechanism ❖ Example ❖ Pathology
, I. ❖ IgE action on mast cells ❖ Hay fever ❖ Mast cell degranulation
results in an inflammatory
response
II. ❖ Tissue-specific ❖ 1-ABO ❖ 1-Complement damages
destruction or incompatibility RBC membrane and cells
impairment because ❖ 5-Graves' disease lyse
of: ❖ 5-Autoantibodies
❖ Antibody binding specific for thyroid tissue
impair receptor for TSH
followed by lysis via
complement
❖ Antibody binding
followed by
macrophage
phagocytosis
❖ Antibody binding
followed by neutrophil
destruction
❖ Antibody-
dependent cell
(NK)-mediated
cytotoxicity, or
❖ Antireceptor
antibodies
III. ❖ Antigen-Antibody ❖ Raynaud’s ❖ Complex deposited in small
complex deposited in phenomenon peripheral vessels in cool
tissues temperatures leading to
vasoconstriction and
blocked circulation
, IV. ❖ Cytotoxic T cell- ❖ Contact ❖ T cells attack tissue
mediated dermatitis (e.g.,
directly (no antibody)
poison ivy)
Edapt Slides Type I: Allergic Reaction
On initial encounter with an allergen, the individual will first produce IgE antibodies. Afte r the
allergen is cleared, the remaining IgE molecules will be bound by mast cells, baso phils, and
eosinophils that contain receptors for the IgE molecules. This process is refer red to as
sensitization. On subsequent exposure to the allergen, the IgE molecules locat ed on the
sensitized cells induces their immediate degranulation. This causes the releas e of inflammatory
mediators such as histamine, leukotrienes, and prostaglandins that re sults in vasodilation,
bronchial smooth muscle contraction, and mucus production. Type I hypersensitivity reactions
can be local or systemic. Systemic reactions can result in an aphylaxis, a potentially life
threatening condition. Allergic asthma is an example of a Type I hypersensitivity reactio
n. On exposure to certain allergens (typically inhaled), individuals with allergic asthma e
xperience inflammation of the airways, characterized by tissue swelling and excessive mucus
production. This narrowing of the airways makes it difficult to breathe.
Type II Hypersensitivity Reaction
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.
• The cell to be destroyed by the antibody
• Cell destruction through phagocytosis by macrophages
• Damage to the cell by neutrophils triggering phagocytosis
• Natural killer cells to release toxic substances that destroy the target cell
• Malfunction of the cell without destruction
, Examples of type II reactions include drug allergies, hemolytic anemia, blood transfusion
mismatch with resulting transfusion reaction and Rh hemolytic disease.
Type III 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-complexes 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.
Type IV 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 characterized by erythema, cellular infiltration and vesicles.
Immunodeficiency
❖ An example of a primary immunodeficiency is: Chronic granulomatous disease (CGD) is
an example of a primary immunodeficiency
❖ Systemic Lupus Erythematosus (SLE) is an example of an autoimmune disease.
❖ Malnutrition is the predominant cause of secondary immune deficiencies worldwide.
❖ A primary immunodeficiency is the result of a single gene defect. It is not usually
inherited; 60% appear within the first two years of life.
MODULE QUESTIONS W ITH EX PERT
SOLUTIONS + RATIONALES
❖ Hives (Urticaria) - Type 1 Allergic Reaction – dermal/skin manifestation.
❖ Allergic Contact Dermatitis – Type 4 Allergic Reaction - an example of a Type IV
hypersensitivity reaction mediated by T-cells. When the individual comes in contact with
the antigen (e.g. 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.
❖ Type 2 (Cytotoxic/tissue-specific) hypersensitivity reactions are mediated by: IgG or IgM.
❖ Which of the following are considered the “first responders” of the innate immune
system? Neutrophils appear first in any immune response.
❖ Anaphylaxis is a Type 1 Allergic Reaction - Type 1 hypersensitivity reactions are
mediated by IgE and mast cells. An individual who is highly sensitized to the antigen may
experience anaphylaxis.
❖ Damage occurs with ABO incompatibility because: Complement damages RBC
membrane causing cell lysis. Damage from ABO incompatibility occurs because of the
effects of complement on the RBC membrane that results in RBC lysis.
❖ 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: anaphylaxis. The
symptoms are consistent with the life-threating condition, anaphylaxis after being
exposed. to a bee sting.
❖ Which of the following assessment findings would be expected in a patient who
presents with urticaria? Eosinophilia. Eosinophils are present in the allergic reaction.
❖ Type IV cytotoxic hypersensitivity reactions are mediated by: T-cells.
❖
Types of Hypersensitivity Reactions
Type ❖ Mechanism ❖ Example ❖ Pathology
, I. ❖ IgE action on mast cells ❖ Hay fever ❖ Mast cell degranulation
results in an inflammatory
response
II. ❖ Tissue-specific ❖ 1-ABO ❖ 1-Complement damages
destruction or incompatibility RBC membrane and cells
impairment because ❖ 5-Graves' disease lyse
of: ❖ 5-Autoantibodies
❖ Antibody binding specific for thyroid tissue
impair receptor for TSH
followed by lysis via
complement
❖ Antibody binding
followed by
macrophage
phagocytosis
❖ Antibody binding
followed by neutrophil
destruction
❖ Antibody-
dependent cell
(NK)-mediated
cytotoxicity, or
❖ Antireceptor
antibodies
III. ❖ Antigen-Antibody ❖ Raynaud’s ❖ Complex deposited in small
complex deposited in phenomenon peripheral vessels in cool
tissues temperatures leading to
vasoconstriction and
blocked circulation
, IV. ❖ Cytotoxic T cell- ❖ Contact ❖ T cells attack tissue
mediated dermatitis (e.g.,
directly (no antibody)
poison ivy)
Edapt Slides Type I: Allergic Reaction
On initial encounter with an allergen, the individual will first produce IgE antibodies. Afte r the
allergen is cleared, the remaining IgE molecules will be bound by mast cells, baso phils, and
eosinophils that contain receptors for the IgE molecules. This process is refer red to as
sensitization. On subsequent exposure to the allergen, the IgE molecules locat ed on the
sensitized cells induces their immediate degranulation. This causes the releas e of inflammatory
mediators such as histamine, leukotrienes, and prostaglandins that re sults in vasodilation,
bronchial smooth muscle contraction, and mucus production. Type I hypersensitivity reactions
can be local or systemic. Systemic reactions can result in an aphylaxis, a potentially life
threatening condition. Allergic asthma is an example of a Type I hypersensitivity reactio
n. On exposure to certain allergens (typically inhaled), individuals with allergic asthma e
xperience inflammation of the airways, characterized by tissue swelling and excessive mucus
production. This narrowing of the airways makes it difficult to breathe.
Type II Hypersensitivity Reaction
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.
• The cell to be destroyed by the antibody
• Cell destruction through phagocytosis by macrophages
• Damage to the cell by neutrophils triggering phagocytosis
• Natural killer cells to release toxic substances that destroy the target cell
• Malfunction of the cell without destruction
, Examples of type II reactions include drug allergies, hemolytic anemia, blood transfusion
mismatch with resulting transfusion reaction and Rh hemolytic disease.
Type III 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-complexes 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.
Type IV 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 characterized by erythema, cellular infiltration and vesicles.
Immunodeficiency
❖ An example of a primary immunodeficiency is: Chronic granulomatous disease (CGD) is
an example of a primary immunodeficiency
❖ Systemic Lupus Erythematosus (SLE) is an example of an autoimmune disease.
❖ Malnutrition is the predominant cause of secondary immune deficiencies worldwide.
❖ A primary immunodeficiency is the result of a single gene defect. It is not usually
inherited; 60% appear within the first two years of life.
