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Micro-Bio Chapter 23
Immune Disorders
| Question | Answer |
|---|---|
| Hypersensitivity | Allergies |
| Type I IgE-Mediated Hypersensitivity | Induced by allergens; person is sensitized as IgE antibodies attach to mast cells and basophils; on subsequent exposures IgE antibodies are cross-linked causing degranulation; includes hay fever, food allergies, asthma, and systemic anaphylaxis |
| Sensitizing | The first dose of antigen; immune system responds as it would to a pathogen |
| Degranulation | Cross-linking of IgE antibodies; releases mediator substances like histamine, leukotrienes, prostaglandins, and cytokines |
| Leukotrienes | Potent smooth muscle constrictors |
| Prostaglandins | Constrict bronchial tubes |
| Cytokines | Stimulate inflammation |
| Systemic Anaphylaxis | Most dangerous form of type I; allergens cause mast cell degranulation + smooth muscle constriction; veins constrict, capillaries expand; fluid forced into tissue, drop in BP, edema, rash, GI cramps, + short breath; lungs fill w/CO2 (death in 10-15 min) |
| Atopic Disorders | The most common form of type I hypersensitivity; a common seasonal allergy caused by inhalation of pollen; year-round allergies result from chronic exposure to allergens |
| Food Allergies | Cause symptoms like swollen lips, abdominal cramps, nausea, diarrhea, hives, and anaphylaxis |
| Physical Factors that Cause Allergies | Extreme temperatures, sunlight, sweating, exercise (asthma) |
| Asthma | Caused by exercise, allergens, or cold temps; degranulation of mast cells release mediators in respiratory tract which causes bronchoconstriction, vasodilation, + mucus buildup; eosinophils + neutrophils in resp tract cause tissue injury + airway blockage |
| Histamine | Is released into the blood; causes smooth muscle cell contraction |
| Only Some have IgE Allergies | Atopic people may not have sufficient IgA which blocks IgE antigen stimulation; they may also have defective suppressor T cells which allow IgE production |
| Expelling Pathogens | Allergies help expel pathogens through sneezing and GI tract contractions |
| Type I Hypersensitivity Therapies | Help control the allergies by identifying the allergen through RAST or ELISA, avoiding the allergen, or desensitization therapy |
| Desensitization Therapy | Involves a series of injections which may cause gradual reduction of granules in mast cells and cause production of IgG antibodies that neutralize antigens, called blocking antibodies |
| Monoclonal Antibodies | Used to dislodge IgE from mast cells and basophils which prevents allergic reactions |
| Antihistamines | Block the effects of histamines |
| Corticosteroids | Are inhaled through the nose to relieve symptoms; some block mediator release |
| Type II Cytotoxic Hypersensitivity | Involves antibody-mediated cell destruction; occurs when IgG reacts with antigens often then activating the complement |
| Agglutination | Occurs if incompatible blood types are mixed; also may activate complement system; can lead to Rh disease |
| Rh Disease | Can lead to stillbirth or jaundice |
| Type III Immune-Complex Hypersensitivity | Caused by antigen-antibody aggregates |
| Serum Sickness | Occurs when IgG is produced against residual proteins in a serum; can cause kidney damage and symptoms of type I anaphylactic hypersensitivity |
| Arthus Phenomenon | Very large amounts of IgG form a complex with antigens which can lead to thromboses in blood vessels |
| Type IV Cellular Hypersensitivity | Mediated by antigen-specific T cells; an exaggeration of cell-mediated immunity; a delayed reaction; causes thickening and drying of skin (induration), and erythema |
| Infection Allergy | Occurs when the immune system responds to certain microbial agents; sensitized lymphocytes stay in tissues to provide immunity for a subsequent infection; sensitivity is determined by injection of a purified microbial sample and observation for induration |
| Contact Dermatitis | Develops after exposure to a variety of allergens; repeated exposures cause drying skin, scaling, and erythema |
| Autoimmune Disorders | Failure to distinguish self from nonself; triggered by gene mutations, if immune system gains access to sterile sites, or if an antigen mimics body substance so the immune system attacks itself (the substance); treatment involves suppressing immune system |
| Myasthenia Gravis | Antibodies react with receptors on muscle fiber membranes which causes a loss in muscle activity |
| Graves Disease | Antibodies bind onto thyroid gland cells causing overproduction of thyroxine |
| Type I Diabetes | Pancreatic beta cells are destroyed causing a lack of insulin production |
| Systemic Lupus Erythematosus (SLE) | AKA lupus; nuclear components of disintegrating WBCs elicit IgG production; immune complexes aggregate in skin and organs causing rash and lesions |
| Rheumatoid Arthritis (RA) | An inflammatory condition resulting in accumulation of immune complexes in joints |
| Autograft | A graft taken from one part of the body and transplanted to another part of the same body |
| Isograft | A graft from one identical twin to the other identical twin |
| Allograft | Grafts between genetically different members of the same species |
| Xenograft | Grafts between members of different species; rarely successful |
| Transplant Rejection | Stimulated by recognition of MHC proteins on surface of graft cells; rejection more likely w/a bigger difference in genetic makeup of donor + recipient; closer the match between donor + recipient, greater the chance of successful transplantation |
| Bone Marrow Transplant | The transplanted marrow can form immune products against the host’s own immune system; cytotoxic T cells attack and destroy transplanted cells; phagocytes secrete lysosomal enzymes that digest the tissue |
| Rejection Inhibition | Inhibition occurs by immunosuppression of the host through steroids that suppress inflammation, antilymphocyte antibodies, antimitotic drugs, and radiation |
| Primary Immunodeficiency | The result of a genetic abnormality |
| Secondary Immunodeficiency | Acquired later in life |
| X-Linked (Bruton) Agammaglobulinemia | A congenital humoral immunodeficiency; B cells fail to develop so patients lack mature B cells, plasma cells and antibodies; a sex-linked trait; more common in males than females |
| DiGeorge Syndrome | The thymus fails to mature in the embryo so T cells do not develop |
| Severe Combined Immunodeficiency Disease (SCID) | Involves lymph nodes deficient in B+ T cells |
| Chediak-Higashi Syndrome | Lysosomes within phagocytes cannot release their contents to kill microbes |
| Chronic Granulomatous Disease | Phagocytes do not produce substances to kill microbes |
| Human Immunodeficiency Virus | Responsible for AIDS; a + RNA virus with reverse transcriptase that copies single strand RNA into double strand DNA |
Created by:
dlnymarie
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