TABLE OF CONTENTS - NR 507 / NR507 Bundle Weeks 1 to 4 Notes Advanc...

Chamberlain University

NR 507 / NR507

Bundle Weeks 1 to 4 Notes Advanced Pathophysiology

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TABLE OF CONTENTS

Week 1 – Immune Response & Hypersensi�vity

Week 2 – Hematologic Disorders & Anemias

Week 3 – Obstruc�ve & Restric�ve Lung Diseases

Week 4 – Urinary System Pathologies & UTIs

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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 3 / 4

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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

Type II Tissue-specific destruction or impairment

because of:

Antibody binding 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

1-ABO incompatibility 5-Graves' disease

1-Complement damages RBC membrane and

cells lyse 5-Autoantibodies specific for thyroid tissue impair receptor for TSH Type IV Cytotoxic T cell-mediated Contact dermatitis (e.g., poison ivy) T cells attack tissue directly (no antibody) Type I IgE action on mast cells Hay fever Mast cell degranulation results in an inflammatory response Type III Antigen-Antibody complex deposited in tissues Raynaud’s phenomenon Complex deposited in small peripheral vessels in cool temperatures leading to vasoconstriction 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.
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