Pathophysiology Test 2 Chapter 9 Alterations of Immunity and Inflammation LATEST EDITION 2024 RATED GRADE A+

Document Content and Description Below

1. Define/differentiate between: A. Allergic Give specific examples of all three and be prepared to defend your answer. Allergy: Definition: Deleterious effects of hypersensitivity to environment ... al antigens. 1. Define/differentiate between: B. Autoimmunity Give specific examples of all three and be prepared to defend your answer. Autoimmunity: Definition: Disturbance in the immunological tolerance of self antigens to the point that the host own tissue are damaged Point out some well known diseases. 1. Define/differentiate between: C. Alloimmunity Give specific examples of all three and be prepared to defend your answer. Alloimmunity: Definition: An individual produces an immunological reaction against the tissues of another person. (Mother against fetus or transplant rejection) 2. Define/differentiate: Type I hypersensitivity reactions See Tables 9-1& 9-3 Type II hypersensitivity reactions Type III hypersensitivity reactions Type VI hypersensitivity reactions Hypersensitivity reactions Mechanism: Four distinct types: 1. Type I IgE mediated through mast cells. 2. Type II Tissue specific reactions, IgG, IgM (See table 9-1) 3. Type III Immune complex reactions. IgG (See table 9-3) 4. Type IV Tissue specific, cell mediated reactions Tc 3. Describe objective 2 in terms of antibodies, target tissues, and cellular components involved in the immune response and be prepared to give examples of each type of hypersensitivity reaction. Hypersensitivity reactions Mechanism: Four distinct types: 1. Type I IgE mediated through mast cells. 2. Type II Tissue specific reactions, IgG, IgM (See table 9-1) 3. Type III Immune complex reactions. IgG (See table 9-3) 4. Type IV Tissue specific, cell mediated reactions Tc 4. Describe the role of Mast cells in the type I hypersensitivity response. Identify the locations where the majority of mast cells reside. Discuss the role of Histamine, Leukotrienes, and Prostaglandin E in type I hypersensitivity reactions Type I- IgE mediated: (See tables 9-1 & 9-3) (See fig 9-1) pages 263-266 1. Involves environmental antigens — called Allergens 2. Repeated exposure to high levels of the antigen. 3. Triggers the production of IgE antibodies rather than IgG or IgM 4. Fc portion of the IgE binds to Mast cells 5. Antigen binds to Fab portion of two adjacent IgE antibodies attached to Mast cells (See fig 9.1 page 267) 6. Repeated allergen exposure triggers massive Mast cell degranulation 7. Histamine binds to H1 and H2 receptors on target cells. 5. What is the role of the two different types of histamine receptors. H1 and H2 . Effects: H1 receptor activation: (See fig 8-1 B page 261) A. Contraction of bronchial smooth muscle B. Increased capillary permeability -----Edema C. Vasodilation, exacerbating edema in throat and Lungs. D. Chemotaxis for eosinophils, then deactivates diapedesis, so they can't leave the inflammatory site. H2 receptor activation: A. Increase gastric secretion B. Decreased mast cell and basophil release of histamine. C. Negative feedback loop control 6. Discuss briefly the value of allergy testing and the use of the flare wheel in diagnosing allergies. Tests for IgE sensitivity: Intradermal skin tests with small amounts of allergens Wheel flare reactions, appear in few minutes, Diameter of the wheel indicates the degree of sensitivity. 7. In true auto-immunity, the body's immune system attacks a tissue that normally should be recognized as self. Explain the type of hypersensitivity each of the following is and how the hypersensitivity damages the tissues. Hasimoto's Disease Diabetes Type I Poison Ivy Contact Dermatitis Lupus Erythematosus Graves Disease Gluten related Celiac Disease Rheumatoid Arthritis Myasthenia Gravis Poison Ivy Contact Dermatitis Type IV Hypersensitivity: (See 9.4 Page 270) Definition: Cell mediated (Tc) or (Td) Lymphokine producing cells, activate the macrophages Doesn't involve antibodies. E.g. Alloimmunity, Graft rejection , Autoimmunity: tumor rejection, Hashimoto's disease, Type I diabetes. Contact dermatitis: Poison oak or Ivy, (See Fig 9-6 page 274) 7. In true auto-immunity, the body's immune system attacks a tissue that normally should be recognized as self. Explain the type of hypersensitivity each of the following is and how the hypersensitivity damages the tissues. Lupus Erythematosus Type III Hypersensitivity: (See fig 9-3 page 269) Definition: Formation of Antigen-antibody complexes in circulation which deposit in organs and tissue. Not organ specific! Mechanism: 1. Formation of Antigen-antibody complexes formed in circulation. Antigen is soluble released into the blood. 2. Deposition of the complex in vessel walls in any organ or tissue. 3. Activation of complement, triggers chemotaxis. 4. Neutrophils try to phagocytize the complexes. 5. Neutrophils degranulate, releasing large quantities of lysozymes causing significant tissue or organ damage. E.g. Lupus, (Systemic Lupus erythematosus) Lupus (Systemic Lupus Erythematosus) (See Fig 9-7 page 277) E.G. if a Type III hypersensitivity antigen antibody complex deposition disease 1. Production of antibodies against Host A. DNA B. Erythrocytes C. Coagulation proteins D. Phospholipids E. Platelets 2. Antigen-Antibody Complexes A. Have a high affinity for the renal glomerular basement membrane due to high filtration rate. Lower for other capillaries, but they also filter. B. Deposit in blood vessels of many organs triggering neutrophils to release lysozymes into the tissue. 3. Blood Vessels lesions in- Kidneys, Choroid plexus, heart, spleen, GI tract, skin and peritoneum. Clinical Manifestations: 1. Facial rash 6. Renal disorders 2. Skin photosensitivity 7. Neural disorders 3. Oral and Nasal ulcers 8. hematologic disorder 4. Arthritic symptoms 9. Immune disorder Definitive diagnosis 5. Pleurisy, pericarditis 10. Antinuclear antibody 7. In true auto-immunity, the body's immune system attacks a tissue that normally should be recognized as self. Explain the type of hypersensitivity each of the following is and how the hypersensitivity damages the tissues. Graves Disease Type II Hypersensitivity: Tissue specific autoimmunity: Definition: Auto-immunity or Allo-immunity Activation of B lymphocytes to produce antibodies, IgG or IgM against a specific antigen that have a particular antigen on its plasma membrane. Specific tissues or cells have MHC markers, but also have unique cell or tissue specific antigens. E.g. platelets. RBC's 4 Tissue effects: 1. Cell destruction, mediated through complement activation ( see fig 9-2) Example: Autoimmune hemolytic anemia Alloimmune, ABO mismatch for transfusion 2. Cell destruction through Phagocytosis. Example Rh+ baby reaction with Rh- mother, mother IgG antibodies bind and cause opsonization, tag RBCs for destruction in the Spleen, Slow anemia develops 3. Antigen-Antibody complex attracts Neutrophils, if cells are endothelial cells, phagocytosis can't occur so neutrophils release lysozymes into the blood. (Very similar to Type III hypersensitivity reaction) but antigens are fixed. 4. Antigen dependent Cell Mediated Cytotoxicity. Activates Tc cells or NK cells once the antibody is attached. Activated by Fc portion of IgG. 5. Does not destroy the target cell, but causes cells to malfunction: Example: Graves disease, (See fig 9-2 E page 268) 7. In true auto-immunity, the body's immune system attacks a tissue that normally should be recognized as self. Explain the type of hypersensitivity each of the following is and how the hypersensitivity damages the tissues. Gluten related Celiac Disease Rheumatoid Arthritis Myasthenia Gravis Targets of Hypersensitivity: What causes the immune systems to attack its own tissues? Haptens: A small foreign molecule (e.g. penicillin) binds to a protein on the cell membrane of the hosts cell. Forming a new antigen called Neoantigens! E.g. Gluten Celiac Disease Penicillin Hemolysis Catechols Poison Ivy, Poison Oak is similar Occurs with penicillin related and sulfonamide antibiotics. Bind to proteins on the membranes of RBC's 7. In true auto-immunity, the body's immune system attacks a tissue that normally should be recognized as self. Explain the type of hypersensitivity each of the following is and how the hypersensitivity damages the tissues. Rheumatoid Arthritis Interaction of the Immune Stress modulators and the immune system: (See fig. 10-4 pg. 346) Cortisol and Norepinephrine, Inhibit Th1 limiting the cellular immune response Norepinephrine Stimulates the Th2 cells, enhancing the Humoral response Cortisol Inhibits Fibroblast proliferation, slowing healing. In summary, Prolonged stress may 1. Increase our susceptibility to Cancer and certain viral infections 2. Worsen Type I hypersensitivity reactions such as asthma and rheumatoid arthritis. 3. Slow healing 7. In true auto-immunity, the body's immune system attacks a tissue that normally should be recognized as self. Explain the type of hypersensitivity each of the following is and how the hypersensitivity damages the tissues. Myasthenia Gravis A weakness and rapid fatigue of muscles under voluntary control. Type II reactions can affect healthy cells. Examples include Red blood cells in Haemolytic Anaemia, Acetylcholine receptors in Myasthenia Gravis, and TSH receptors in Grave's Disease. Hasimoto's Disease immune system attacks thyroid; most common cause of hypothyroidism in the US Diabetes Type I not enough insulin, in rare cases can be caused by an autoimmune disease Lupus Erythematosus Autoimmune disorder characterized by a red, scaly rash on the face and upper trunk Graves Disease A condition of unknown origin that involves the throid gland and causes the soft tissues surrounding the globe to swell. (proptosis) Autoantibody (IgG) that stimulates TSH receptor (type II hypersensitivity) Autoimmune disorder where the immune system produces antibodies that bind to the receptor for TSH and activate sustained thyroid hormone production. The most common hyperthyroidism. Gluten related Celiac Disease Celiac disease is an autoimmune disorder in which the body mistakenly reacts to gluten, a protein found in wheat, barley and rye, as if it were a poison. Rheumatoid Arthritis Anti-IgG antibodies A chronic inflammatory diease that causes joint pain, swelling, and stiffness. Most common in women and can occur at any age. Some persons need joint replacement surgery Myasthenia Gravis A disease in which acetylcholine receptors on muscle cells are destroyed so that muscles can no longer respond to the acetylcholine signal to contract. Symptoms include muscular weakness and progressively more common bouts of fatigue. The disease's cause is unknown but is more common in females than in males; it usually strikes between the ages of 20 and 50. Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: A. Neoantigens 2. Neoantigens! New antigens on a cell surface produced by: A. Mutations of DNA producing membrane bound proteins. B. Viral infected cells producing membrane bound viral proteins C. Fetal or embryonic antigens produced by cancer cells undergoing reverse differentiation. Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: B. Haptens Haptens: A small foreign molecule (e.g. penicillin) binds to a protein on the cell membrane of the hosts cell. Forming a new antigen called Neoantigens! E.g. Gluten Celiac Disease Penicillin Hemolysis Catechols Poison Ivy, Poison Oak is similar Occurs with penicillin related and sulfonamide antibiotics. Bind to proteins on the membranes of RBC's Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: C. Sequestered Antigens 1. Sequester antigens: Self antigens located in "Immunological privileged sites e.g. testicular area, Spermatozoa, cornea, and Lens of the eyes. Since embryonic exposure did not occur, traumatic injury to the area causing exposure to the immune system will activate the immune system against these tissue since tolerance was never developed. If Type II hypersensitivity occurs because of damage to one eye with consequent exposure to an immune response, the other cornea is also at risk since antibodies will attach both corneas! Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: D. Viral infections 6. Viruses: A. Viral infected cells may produce virally induced antigens on the plasma membranes. E.g. Rubella induced encephalitis. Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: E. Infectious diseases 3. Infectious diseases: A. Formation of immune complexes with endotoxins which precipitate in organs or tissues. (Kidney failure results from deposition of immune complexes) B. Introduction of a antigen so closely resembling a self antigen that the activated antibodies will bind to both the foreign and self antigens. E.g. Rheumatic fever from Streptococcus A bacteria. Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: F. Forbidden clones 4. Forbidden clones: A. Embryonic clones that developed but were suppressed , but some of the cloned b lymphocytes survived and proliferate later in life. Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: G. Spontaneous mutations possible neoantigens? Be prepare to discuss the role of each of the following in the erroneous auto-immune responses. Define and differentiate the following: H. Failure of T reg cells G. Treg lymphocytes 5. Suppressor T cell dysfunction: Loss or dysfunction of an antigen specific colony of Ts cells. Which have been providing peripheral tolerance suppressing a forbidden clone of B or T lymphocytes made against a self antigen. 8. Explain possible causes of immunno-deficiencies and differentiate between: A. Congenital Two categories: 1. Congenital Chief cause is a disruption of the lymphocyte function. A. Stem cell defect for either B or T lymphocytes or both. B. Lymphoid tissue function disorder, abnormal development of lymphocytes C. Hyperactive Ts (Suppressor lymphocytes) (See table 8-6) 8. Explain possible causes of immunno-deficiencies and differentiate between: B. Acquired 2. Secondary (Acquired) immune deficiencies (See list page 284) a. Infections, rubella, measles, leprosy, tuberculosis, b. Malignancies: Hodgkins disease and leukemia c. Chemotherapy or Radiation therapy for Cancer c. Stress d. Malnutrition, low Proteins, calories, iron or zinc (Cofactor for 70 different enzymes, many of which are in lymphocytes.) e. Aging [Show More]

Last updated: 1 year ago

Preview 4 out of 12 pages