Chamberlain University
NR 507 / NR507
Bundle
Weeks 1 to 4 Notes
Advanced Pathophysiology
,TABLE OF CONTENTS
Week 1 – Immune Response & Hypersensitivity
Week 2 – Hematologic Disorders & Anemias
Week 3 – Obstructive & Restrictive Lung Diseases
Week 4 – Urinary System Pathologies & UTIs
, lOMoAR cPSD| 51648332
Week 1: Immune Response
Type I: 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 cells induces their immediate degranulation. This causes the release of inflammatory
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.
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
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
Downloaded by Benjamin Luca ()
, lOMoAR cPSD| 51648332
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.
Type Mechanism Example Pathology
Tissue-specific
destruction or impairment
because of:
Antibody binding followed
by lysis via complement
Antibody binding followed 1-Complement damages RBC membrane and
1-ABO
Type by macrophage incompatibility
cells lyse
II phagocytosis 5-Autoantibodies specific for thyroid tissue impair
5-Graves' disease
Antibody binding followed receptor for TSH
by neutrophil destruction
Antibody-dependent cell
(NK)-mediated
cytotoxicity, or
Antireceptor antibodies
Type Contact dermatitis
Cytotoxic T cell-mediated T cells attack tissue directly (no antibody)
IV (e.g., poison ivy)
Type Mast cell degranulation results in an
IgE action on mast cells Hay fever
I inflammatory response
Complex deposited in small peripheral vessels in
TypeAntigen-Antibody complex Raynaud’s
cool temperatures leading to vasoconstriction
III deposited in tissues phenomenon
and blocked circulation
Hives
Hives (urticaria) are an example of a:
- Type 1 hypersensitivity reaction.
- Type 2 hypersensitivity reaction.
- Type 3 hypersensitivity reaction.
- Type 4 hypersensitivity reaction.
Anaphylaxis is a type 1 hypersensitivity reaction.
Immune System
Which of the following are considered the “first responders” of the innate immune system?
- Eosinophils.
- IgM.
Downloaded by Benjamin Luca ()
NR 507 / NR507
Bundle
Weeks 1 to 4 Notes
Advanced Pathophysiology
,TABLE OF CONTENTS
Week 1 – Immune Response & Hypersensitivity
Week 2 – Hematologic Disorders & Anemias
Week 3 – Obstructive & Restrictive Lung Diseases
Week 4 – Urinary System Pathologies & UTIs
, lOMoAR cPSD| 51648332
Week 1: Immune Response
Type I: 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 cells induces their immediate degranulation. This causes the release of inflammatory
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.
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
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
Downloaded by Benjamin Luca ()
, lOMoAR cPSD| 51648332
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.
Type Mechanism Example Pathology
Tissue-specific
destruction or impairment
because of:
Antibody binding followed
by lysis via complement
Antibody binding followed 1-Complement damages RBC membrane and
1-ABO
Type by macrophage incompatibility
cells lyse
II phagocytosis 5-Autoantibodies specific for thyroid tissue impair
5-Graves' disease
Antibody binding followed receptor for TSH
by neutrophil destruction
Antibody-dependent cell
(NK)-mediated
cytotoxicity, or
Antireceptor antibodies
Type Contact dermatitis
Cytotoxic T cell-mediated T cells attack tissue directly (no antibody)
IV (e.g., poison ivy)
Type Mast cell degranulation results in an
IgE action on mast cells Hay fever
I inflammatory response
Complex deposited in small peripheral vessels in
TypeAntigen-Antibody complex Raynaud’s
cool temperatures leading to vasoconstriction
III deposited in tissues phenomenon
and blocked circulation
Hives
Hives (urticaria) are an example of a:
- Type 1 hypersensitivity reaction.
- Type 2 hypersensitivity reaction.
- Type 3 hypersensitivity reaction.
- Type 4 hypersensitivity reaction.
Anaphylaxis is a type 1 hypersensitivity reaction.
Immune System
Which of the following are considered the “first responders” of the innate immune system?
- Eosinophils.
- IgM.
Downloaded by Benjamin Luca ()
