19 terms

Chapter 8: Clinical Scenarios and Critical Thinking Questions

Test 3- Alterations in Immunity and Inflammation
What happens during a type I hypersensitivity reaction? Indicated responses to major mediators.
Ans: IgE antibodies (from previous sensitization) attached to mast cells. The allergen should have two antigenic determinants to interact with two IgE-Fc eceptor complexes. This interaction results in the degranulation of the mast cells, thus releasing presynthesized and synthesized mast cell products

Clinical Manifestations of Type I Hypersensitivity Reactions:
Gastrointestinal: vomiting, diarrhea, abdominal pain, malabsorption
Skin: urticaria, itching, angioedema
Respiratory: conjunctivitis, rhinitis, bronchospasm, asthma, laryngeal edema
Cardiovascular: hypotension, tachycardia, dysrhythmias
Analyze the difference between the antigen-antibody reaction in a type II hypersensitivity reaction and a type III hypersensitivity reaction. Give an example of each type of reaction.
Ans: Type Hypersensitivity reaction is also known as tissue-specific, cytotoxic or cyolytic hypersensitivity reaction. It is characterized by antibodies that attack antigens on the surface of specific cells or tissues. The reaction is organ specific. This antigen-antibody reaction is immediate, occurring within 15 to 30 minutes after exposure to the antigen. IgG and IgM are the principal antibodies. It is mediated by the complement system and a variety of principal effector cells, including tissue macrophages, platelets, killer cells, neutrophils, and eosinophils. The symptoms are related to the antigenic target of the antibody. Examples of the hypersensitivity reaction include ABO transfusion reactions, hemolytic disease of the newborn, MG, throiditis, hyperacute graft rejections, and autoimmune hemolytic anemias.

Type III hypersensitivity reaction is also known as immune complex or Arthus disease. This reaction is a sequential process beginning with an interaction between a soluble antigen and soluble antibody. It is characterized by antigen-antibody complex formation that usually occurs in the circulation. The complex is then deposited into vascular walls or extravascular tissues, causing an inflammatory reaction. The reaction is not organ specific and peaks 6 hours after exposure to the antigen. IgG is the principal antibody. The principal effector cells include neutrophils and mast cells. Examples of this type of hypersensitivity reaction include serum sickness, glomerulonephritis, systemic lupus erythematosus, rheumatoid arthritis, drug-induced vasculitis, and polyarteritis nodosa.
Explain how vaccines work.
Ans: Vaccines prevent disease by inducing a primary and secondary immune response under conditions that will not result in disease. Vaccines exist to prevent certain viral and bacterial infections. Viral vaccines usually contain attenuated lives viruses, but most bacterial vaccines contain killed organisms or bacterial antigens. The primary immune response from vaccines is usually short-lived, so booster injections are given to produce multiple secondary responses resulting in a large number of memory cells and long-lasting active immunity.
Mr. Jones was attending a family birthday party and ate some delicious casserole during the picnic. He is allergic to shellfish but was not told by the host that the casserole did not contain any seafood. All of a sudden he started having abdominal cramps and breathing difficulties. Explain the process of anaphylaxis.
Ans: Anaphylaxis occurs when a hypersensitivity reaction is extremely severe. It happens within minutes of the reexposure to the antigen. In this case it would be considered systemic anaphylaxis. Unless treated quickly it can result in death.
What is the safest way to test for a particular allergen?
Ans: The safest ways to test for an allergen is either as an injection, intradermally, or as a skin test. Giving small amounts of a food allergen is considered dangerous if the person has a history of an anaphylactic response. Skin tests are contraindicated in individuals with dermatitis because it would be difficult to interpret the reaction on the skin.
Explain the treatments available for systemic lupus erythematosus (SLE).
Ans: Unfortunately there is no cure for SLE- the goal should be to control the symptoms and to prevent further damage. Treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppresive drugs, and protection from sunlight.
Hypersensitivity is best defined as a(n):
Ans: Altered immunologic response to an antigen that results in disease.
Exp: Hypersensitivity is an altered immunologic response to an antigen that results in disease or damage to the host.
The hypersensitivity reaction that occurs after a person who is allergic to bee stings is stung by a bee is called:
Ans: Anaphylaxis
Exp: Examples of systemic anaphylaxis are allergic reactions to bee stings, peanuts, and fish.
Common hay fever allergy is expressed through a reaction that is mediated by:
Ans: IgE
Exp: Type I reactions are mediated by antigen-specific IgE and the products of tissue mast cells. 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.
Te class of antibody involved in type I hypersensitivity reaction is:
Ans: IgE
Exp: Type I reactiosn are mediated by antigen-specific IgE and the products of tissue mast cells
Blood transfusion reactions are an example of:
Ans: Alloimmunity
Exp: Alloimmunity (also termed isoimmunity) occurs when the immune system of one individual produces an immunologic reaction against tissues of another individual.
Durin an IgE-mediated hypersensitivity reaction, which leukocyte is activated?
Ans: Eosinophils
Exp: Another important activity of histamine is enhancement of the chemotactic activity of other factors, such as eosinophil chemotactic factor of anaphylaxis (ECF-A), which attracts eosinophils into sites of allergic inflammatory reactions and prevents them from migrating out of the inflammatory site.
During an IgE-mediated hypersensitivity reaction, what causes bronchospasm?
Ans: Smooth muscle contraction caused by histamine bound to H1 receptors
Exp: Acting through the H1 receptors, histamine contracts bronchial smooth muscles, causing bronchial constriction; increases vascular permeability, causing edema; and causes vasodilator, increasing blood flow to the affected area.
What is a characteristic of atopic individuals who are genetically predisposed to develop allergies?
Ans: They produce greater quantities of IgE than other individuals.
Exp: Atopic individuals tend to produce higher quantities of IgE and to have more Fc receptors for IgE on their mast cells.
What is the mechanism in type II hypersensitivity reactions?
Ans: Antibodies bind to the antigens on the cell surface
Exp: All of these mechanisms begin with antibody binding to tissue specific antigens or antigens that have attached to particular tissues. First, the cell can be destroyed by antibody (IgG or IgM) and activation of the complement cascade through the classical pathway.
In type II hypersensitivity reaction, when antibodies are formed against red blood cell antigens of the Rh system, the blood vessels are destroyed by:
Ans: Phagocytosis in the spleen
Exp: Antibodies against platelet-specific antigens or against red blood cell antigens of the Rh system coat those cells at low density, resulting in their preferential removal by phagocytosis in the spleen, rather than by complement-mediated lysis.
In a type II hypersensitivity reaction, when soluble antigens from infectious agents enter circulation, tissue damage is a result of:
Ans: Neutrophil granules and toxic oxygen products
Exp: The components of neutrophil granules, as well as the several toxic oxygen products produced by these cells, damage the tissue
What is the mechanism in type III hypersensitivity reactions?
Ans: Antibodies bind to soluble antigens that were released into body fluids and the immune complexes are deposited in the tissues.
Exp: Most type III hypersensitivity diseases are caused by antigen-antibody (immune) complexes that are formed in the circulation and deposited later in vessel walls or extravascular tissues.
What is the mechanism in type IV hypersensitivity reactions?
Ans: Cytotoxic T lymphocytes or lymphokine-producing Th1 cells attack and destroy cellular targets directly.
Exp: Whereas types I,II, and III hypersensitivity reactions are mediated by antibody, type IV reactions are mediated by T lymphocytes and do not involve antibody. Type IV mechanisms occur through either cytotoxic T lymphocytes (Tc cells) or lymphokine-producing Th1 cells. Tc cells attack and destroy cellular targets directly.