Patho

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Patho
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  1. What is innate immunity?
    Innate immunity, also known as natural or native immunity, includes natural barriers (physical, mechanical, and biochemical) and inflammation. they are the first line of defense and are placed on the body surfaces at birth
  2. what is the time it takes for adaptive or acquired immunity takes to work?
    Delay between primary exposure to antigen and maximal response; immediate against secondary exposure to antigen
  3. what is the specificity of adaptive immunity?
    Response is very specific toward “antigen”
  4. what are the cells for innate immunity?
    Mast cells, granulocytes (neutrophils, eosinophils, basophils), monocytes/ macrophages, natural killer (NK) cells, platelets, endothelial cells
  5. what are the active molecules for adaptive immunity?
    antibodies
  6. In innate immunity what is the first line of defense?
    The physical barriers that cover the external parts of the human body offer considerable protection from damage and infection. These barriers are composed of tightly associated epithelial cells.
  7. Where are the physical barriers found?
    on the skin and the linings of the gastrointestinal, genitourinary, and respiratory tracts
  8. what happens when a pathogen comes in contact with the physical barriers?
    may be removed by mechanical means—sloughed off with dead skin cells, expelled by coughing or sneezing, vomited from the stomach, or flushed from the urinary tract by urine. in the respiratory tract mucus is created and have cilia that trap and move things up and out
  9. What is normal flora?
    • A spectrum of nonpathogenic microorganisms, collectively called the normal flora, resides on the body's surfaces.
    • -combination of mostly bacteria and occasionally fungi that is unique to the particular location
  10. where do you find normal flora?
    skin and the mucous membranes of the eyes, upper and lower gastrointestinal tracts, urethra, and vagina
  11. What does a commensal organism mean?
    • - what normal floral is most referred to as
    • to the benefit of one organism without affecting the other
  12. the the natural flora relationship with humans?
    the relationship with humans may be more mutualistic (to the benefit of both organisms)
  13. how is the colon an example of normal flora?
    at birth the lower gut is relatively sterile, but colonization with bacteria begins quickly, with the number, diversity, and concentration increasing progressively
  14. what does the flora in the colon do to help?
    The environment of the intestine provides the needed temperature and nutrients for the growth of many bacterial species. To the benefit of humans, many of these microorganisms help digest fatty acids, large polysaccharides, and other dietary substances and absorb ions.
  15. Does normal flora produce chemicals?
    Yes! they produce chemicals (ammonia, phenols, indoles, and other toxic materials) and toxic proteins (bacteriocins) that inhibit colonization by pathogenic microorganisms.
  16. what happens to normal flora when you take antibiotics?
    treatment with broad-spectrum antibiotics can alter normal intestinal flora, decreasing its protective activity, and lead to overgrowth of pathogenic microorganisms, such as the yeast Candida albicans or the bacteria Clostridium difficile
  17. What is Lactobacillus?
    The bacterium Lactobacillus is a major constituent of the normal vaginal flora in healthy women.
  18. what does the bacterium lactobacillus do?
    produces chemicals (hydrogen peroxide, lactic acid, and other molecules) that help prevent infections of the vagina and urinary tract by other bacteria and yeast.
  19. what happens if your floral on your vagina diminishes?
    Diminished colonization with lactobacilli (e.g., as a result of prolonged antibiotic treatment) increases the risk for urologic or vaginal infections, such as vaginosis.
  20. what are opportunistic microorganism?
    they can cause disease if the individual's defenses are compromised. These organisms are normally controlled by the innate and acquired immune systems and contribute to our defenses.
  21. what is an example of an opportunistic microorganism?
    Pseudomonas aeruginosa is part of the normal flora on skin it produces a toxin that protects against infections with staphylococcal and other bacteria. However, severe burns compromise the integrity of the skin and may lead to life-threatening systemic pseudomonal infections.
  22. What is the second line of defense in innate immunity?
    The innate immune system is programmed to respond to damage to the body. the response initiates an interactive system of humoral (soluble in the blood) and cellular systems, called inflammation.
  23. what is the first response to injury?
    inflammation
  24. where does the inflammatory response occur?
    occurs in tissues with a blood supply (vascularized)
  25. what does inflammation depend on?
    depends on the activity of both cellular and chemical components
  26. is inflammation specific or nonspecific? and why?
    nonspecific, meaning that it takes place in approximately the same way regardless of the type of stimulus or whether exposure to the same stimulus has occurred in the past
  27. what are symptoms of inflammation?
    The classic symptoms of acute inflammation include redness (erythema), heat, swelling, pain, and loss of function.
  28. what is Microscopic inflammatory?
    changes occur within seconds in the microcirculation (arterioles, capillaries, and venules) near the site of an injury
  29. what are the processes of microscopic inflammation?
    • 1.Vasodilation (increased size of the blood vessels), causes slower blood velocity and increases blood flow to the injured site
    • 2.Increased vascular permeability (the blood vessels become porous from contraction of endothelial cells) and leakage of fluid out of the vessel, causing swelling (edema) at the site of injury
    • 3.White blood cell adherence to the inner walls of vessels and their migration through enlarged junctions between the endothelial cells lining the vessels into the surrounding tissue
  30. What are the benefits to inflammation?
    • -Prevents infection and further damage
    • -Limits and control the inflammatory process through the influx of plasma protein systems 
    • -Interacts with components of the adaptive immune system to elicit a more specific response to a pathogen
    • -Prepares area of injury for healing by removal of bacterial products, dead cells, and other products of inflammation
  31. what happens to the stuff that accumulates at the inflamed site?
    Fluid and debris that accumulate at an inflamed site are drained by lymphatic vessels. This process also facilitates the development of acquired immunity
  32. what are the three key plasma protein systems are essential to an effective inflammatory response
    These are the complement system, the clotting system, and the kinin system. they preform diff things but all have similarities
  33. what are the similarities of the plasma protein systems?
    Each consists of multiple proteins in the blood. They're normally in inactive forms; several are enzymes that circulate in inactive forms as proenzymes. Each system contains proteins that can be activated during inflammation.
  34. what is a the complement cascade, the clotting cascade, or the kinin cascade?
    Activation of the first components results in sequential activation of other components of the system, leading to a biologic function that helps protect the individual. This sequential activation is referred to as a cascade
  35. what is the complement system?
    it consists of a large number of proteins (sometimes called complement factors) that together constitute about 10% of the total circulating serum protein.
  36. why is the complement system important?
    its extremely important because activation produces factors that can destroy pathogens directly or can activate or increase the activity of many other components of the inflammatory and adaptive immune response
  37. how strong are the factors that are produced during complement system?
    Factors produced during activation of the complement system are among the body's most potent defenders against bacterial infection
  38. What is C3 and C5?
    The most important function of the complement cascade is activation of C3 and C5, which results in a variety of molecules that are (1) opsonins, (2) chemotactic factors, or (3) anaphylatoxins.
  39. what are opsonins?
    Opsonins coat the surface of bacteria and increase their susceptibility to being phagocytized (eaten) and killed by inflammatory cells, such as neutrophils and macrophages
  40. what are chemotactic factors?
    Chemotactic factors diffuse from a site of inflammation and attract phagocytic cells to that site.
  41. what are anaphylatoxins?
    they induce rapid degranulation of mast cells (i.e., release of histamine that induces vasodilation and increased capillary permeability), a major cellular component of inflammation.
  42. what is the clotting system?
    The clotting (coagulation) system is a group of plasma proteins that, when activated sequentially, form a blood clot
  43. what is a blood clot?
    A blood clot is a meshwork of protein (fibrin) strands that stabilizes the platelet plug and traps other cells, such as erythrocytes, phagocytes, and microorganisms
  44. What do clots do?
    Clots (1) plug damaged vessels and stop bleeding, (2) trap microorganisms and prevent their spread to adjacent tissues, and (3) provide a framework for future repair and healing
  45. how is the clotting system activated?
    The clotting system can be activated by the tissue factor (extrinsic) pathway and the contact activation (intrinsic) pathway
  46. What do the routes of the clotting initiation lead to?
    All routes of clotting initiation lead to activation of factor X and thrombin. Thrombin is an enzyme that proteolytically activates fibrinogen to form fibrin and small fibrinopeptides (FPs)
  47. what does fibrin do?
    Fibrin polymerizes to form a clot, and the FPs are highly active as chemotactic factors and causing increased vascular permeability
  48. what is XIIa?
    The XIIa produced by the clotting system can also be activated by kallikrein of the kinin system
  49. What is the kinin system?
    The third plasma protein system, the kinin system, interacts closely with the coagulation system
  50. what happens in the kinin system?
    Prekallikrein is enzymatically converted to kininogen, which activates bradykinin. Bradykinin functions similar to histamine and increases vascular permeability.
  51. what  is the final product of the kinin system?
    The final product of the kinin system is a small-molecular-weight molecule, bradykinin, which is produced from a larger precursor molecule, kininogen
  52. What does bradykinin do?
    Bradykinin causes dilation of blood vessels, acts with prostaglandins to induce pain, causes smooth muscle cell contraction, and increases vascular permeability.
  53. what does the formation of clots also activate?
    clots also activates a fibrinolytic system that is designed to limit the size of the clot and remove the clot after bleeding has ceased
  54. what does thrombin activate?
    Thrombin of the clotting system activates plasminogen in the blood to form the enzyme plasmin
  55. what does plasmin do?
    The primary activity of plasmin is to degrade fibrin polymers in clots
  56. what are interleukins?
    Interleukins (ILs) are produced predominantly by macrophages and lymphocytes in response to stimulation of PRRs or by other cytokines
  57. what do interleukins?
    Attraction of leukocytes to a site of inflammation (chemotaxis)
  58. What is interleukin-1
    Interleukin-1 (IL-1) is produced mainly by macrophages. It activates monocytes, other macrophages, and lymphocytes, thereby enhancing both the innate and acquired immunity. IL-1 is an endogenous pyrogen (i.e., fever-causing cytokine)
  59. what is degranulation?
    • the release of the contents of mast cell granules
    • In response to a stimulus, biologically active molecules are released from the mast cell granules within seconds and exert their effects immediately. These molecules include histamine and chemotactic factors.
  60. what is a histamine?
    • Histamine is a small-molecular-weight molecule with potent effects on many other cells, particularly those that control the circulation
    • -histamine and serotonin are called a vasoactive amine
  61. what do histamines cause?
    • These molecules cause temporary, rapid constriction of smooth muscle and dilation of the postcapillary venules, which results in increased blood flow into the microcirculation
    • -it also causes increased vascular permeability
  62. what do mast cells contain?
    Mast cell granules also contain chemotactic factors, two of which are neutrophil chemotactic factor (NCF)
  63. what is the functionof prostaglandins?
    Prostaglandins cause increased vascular permeability, neutrophil chemotaxis, and pain by direct effects on nerves
  64. what is the endothelium?
    The vessel walls consist of a layer of endothelial cells that adhere to an underlying matrix of connective tissue. The matrix contains a variety of proteins, including collagen, fibronectin, and laminins
  65. what do endothelial cells do?
    Endothelial cells regulate circulating components of the inflammatory system and maintain normal blood flow by preventing spontaneous activation of platelets and members of the clotting system
  66. what do endothelial cells produce?
    Endothelial cells produce nitric oxide (NO) from arginine and prostacyclin (PGI2) from arachidonic acid
  67. what do both NP and PGI2 do?
    Both NO and PGI2 maintain blood flow and pressure and inhibit platelet activation. PGI2 and NO are synergistic
  68. what does NO do?
    NO is released continually to relax vascular smooth muscle and suppress the effects of low levels of cytokines, thus maintaining vascular tone
  69. What does PGI2 do?
    PGI2 production varies a great deal and is increased when additional regulation is needed.
  70. what happens to the damage endothelial cell lining?
    Damage to the endothelial cell lining of the vessel exposes the subendothelial connective tissue matrix, which is prothrombogenic and initiates platelet activation and formation of clots
  71. what are platelets?
    Platelets are cytoplasmic fragments formed from megakaryocytes. They circulate in the bloodstream until vascular injury occurs
  72. what happens to platelets after injury?
    After injury, platelets are activated by many products of tissue destruction and inflammation, including collagen, thrombin, and platelet-activating factor
  73. what does the activation of platelets result in?
    • (1) their interaction with components of the coagulation cascade to stop bleeding
    • (2) degranulation, releasing biochemical mediators such as serotonin, which has vascular effects similar to those of histamine
  74. platelets and growth factors?
    Platelets also release growth factors that promote wound healing
  75. what is a neutrophil?
    The neutrophil, or polymorphonuclear neutrophil (PMN), is a member of the granulocytic series of white blood cells and is named for the characteristic staining pattern of its granules as well as its multilobed nucleus
  76. how are neutrophils involved in injury?
    Neutrophils are the predominant phagocytes in the early inflammatory site, arriving within 6 to 12 hours after the initial injury
  77. what are macrophages?
    the mature cell in the tissues
  78. what are monocytes?
    the immature form of this white blood cell in the blood
  79. what do monocytes and macrophages have in common?
    have fewer and larger lysosomes in their cytoplasm than do granulocytes
  80. what is the process of phagocytosis?
    The process that results in phagocytosis is characterized by three interrelated steps: adherence and diapedesis, tissue invasion by chemotaxis, and phagocytosis
  81. what is phagocytosis?
    Phagocytosis is the process by which a cell ingests and disposes of foreign material, including microorganisms.
  82. What are the cells called that preform phagocytosis?
    Phagocytes
  83. what are the 2 most important phagocytes?
    neutrophils and macrophages
  84. What are characteristics of acute inflammation? and why do they come about?
    All the local characteristics of acute inflammation (i.e., swelling, pain, heat, and redness [erythema]) result from vascular changes and the subsequent leakage of circulating components into the tissue
  85. what is serous exudate?
    In early or mild inflammation, the exudate is watery (serous exudate) with very few plasma proteins or leukocytes
  86. What is purulent (suppurative) exudate?
    If a large number of leukocytes accumulate, as in persistent bacterial infections, the exudate consists of pus and is called a purulent (suppurative) exudate. Purulent exudate is characteristic of walled-off lesions (cysts or abscesses).
  87. what is hemorrhagic exudate?
    If bleeding occurs, the exudate is filled with erythrocytes and is described as a hemorrhagic exudate.
  88. what is leukocytosis?
    Leukocytosis is an increase in the number of circulating white blood cells. During many infections, leukocytosis may be accompanied by a left shift in the ratio of immature to mature neutrophils
  89. what is chronic inflammation?
    chronic inflammation lasts 2 weeks or longer, regardless of cause
  90. what is primary intention?
    Wounds that heal under conditions of minimal tissue loss are said to heal by primary intention
  91. what is secondary intention healing?
    Healing of an open wound, such as a stage IV pressure ulcer (decubitus ulcer), requires a great deal of tissue replacement so that epithelialization, scar formation, and contraction take longer and healing occurs through secondary intention
  92. what is granulation tissue? what is it filled with?
    it grows into the wound from surrounding healthy connective tissue. Granulation tissue is filled with new capillaries (angiogenesis) derived from capillaries in the surrounding tissue, giving the granulation tissue a red, granular appearance.
  93. What is dysfunctional wound healing?
    Dysfunctional wound healing and impaired epithelialization may occur during any phase of the healing process.
  94. what causes dysfunctional wound healing?
    causes includes ischemia, excessive bleeding, excessive fibrin deposition, a predisposing disorder such as diabetes mellitus, wound infection, inadequate nutrients, numerous drugs, and tobacco smoke.
  95. what is oxygen-deprived tissue?
    Oxygen-deprived (ischemic) tissue is susceptible to infection, which prolongs inflammation and delays healing
  96. what does ischemia do?
    Ischemia reduces energy production and impairs collagen synthesis and the tensile strength of regenerating connective tissue.
  97. People with diabetes and wound healing
    they are risk for prolonged wound healing. Wounds are often ischemic because of the potential for small-vessel diseases that impair the microcirculation and alter (glycosylated) hemoglobin, which has an increased affinity for oxygen and thus does not readily release oxygen in tissues.
  98. optimal nutrition
    Optimal nutrition is important during all phases of healing because metabolic needs increase.
  99. what delays wound healing?
    Medications, including antineoplastic (anticancer) agents, nonsteroidal anti-inflammatory drugs (NSAIDs), and steroids, delay wound healing
  100. what does an immune system do?
    The immune system is capable of identifying substances that are foreign, or nonself
  101. what are antigens?
    substances that react with molecules of the immune system (antibodies, receptors on B and T cells) are called antigens
  102. where are antigens found?
    Antigens are on infectious agents (e.g., viruses, bacteria, fungi, or parasites), on noninfectious substances from the environment (e.g., pollens, foods, or bee venoms), or on drugs, vaccines, transfusions, and transplanted tissues
  103. What are antibodies?
    The products of the adaptive immune response include a type of serum protein—immunoglobulins (Ig) or antibodies—and a type of blood cell—lymphocytes
  104. What are antibodies?
    Antibodies are proteins that are produced by B cells, circulate in the blood, and bind to antigens on infectious agents
  105. genetic makeup and immune systems?
    the genetic makeup of the individual can play a critical role in the immune system's ability to respond to many antigens
  106. what is Ig?
    The term immunoglobulin (Ig) is generally used for all antibodies, whereas the term antibody is mostly used to denote one particular set of immunoglobulins known to have specificity for a particular antigen
  107. what are the 5 classes of immunoglobulins?
    There are five classes of immunoglobulins (IgG, IgA, IgM, IgE, and IgD), which are characterized by differences in structure and function
  108. What is IgG?
    its the most abundant class of immunoglobulins, constituting 80% to 85% of the immunoglobulins in the blood and accounting for most of the protective activity against infections. As a result of selective transport across the placenta, maternal IgG is the major class of antibody found in blood of the fetus and newborn
  109. What is IgA?
    IgA has two subclasses: IgA1 and IgA2. IgA1 is found predominantly in the blood, whereas IgA2 is the predominant class found in body secretions
  110. What is IgM?
    its the largest immunoglobulin and usually exists as a pentamer (a molecule consisting of five identical smaller molecules) that is stabilized by a J chain. It is the first antibody produced during the initial, or primary, response to antigens
  111. what is a monoclonal antibody?
    Monoclonal antibody is produced in the laboratory from one B cell that has been cloned; thus all the antibody is of the same class, specificity, and function
  112. what are the advantages of monoclonal antibodies?
    (1) a single antibody of known antigenic specificity is generated rather than a mixture of different antibodies; (2) they have a single, constant binding affinity; (3)they can be diluted to a constant titer (concentration in fluid) because the actual antibody concentration is known; and (4) the antibody can be easily purified
  113. What is IgE?
    IgE is a special class of antibody that protects the individual from infection with large parasites.
  114. what is MHC?
    Major histocompatibility complex (MHC) molecules are glycoproteins found on the surface of all human cells except red blood cells
  115. What is an example of skins normal flora?
    Staphylococcus epidermidis
  116. What are some examples of the distal intestines normal flora?
    lactobacilli, anaerobic bacteria, and C. albicans
  117. what are examples of the colons normal flora?
    Klebsiella, Pseudomonas, and Escherichia coli
  118. What is an example of the norma flora in the vagina?
    Lactobacillus acidophilus
  119. what is pathogenicity?
    Pathogenicity: Ability of an agent to produce disease
  120. what is virulence?
    Virulence: Capacity of a pathogen to cause severe disease
  121. what microorganism causes the tissue damage to form tonsillitis?
    Streptococcus pyogenes
  122. what is the microorganism that cause tissue damage and causes Gram-negative sepsis
    Escherichia coli
  123. what is the microorganism that causes tissue damage and causes you to have wound infections?
    Pseudomonas aeruginosa
  124. whats the microorganism that cause cold sores?
    Herpes simplex virus
  125. What do gram stains and acid-fast stains do?
    Gram stain and acid-fast stain are important for differentiating gram-positive or gram-negative types of bacteria
  126. what is bacteremia?
    Bacteremia is the presence of bacteria in the blood
  127. What is septicemia?
    septicemia is growth of bacteria in the blood and is caused by a failure of the body's defense mechanisms
  128. what are mycoses?
    Diseases caused by fungi are called mycoses. Mycoses can be superficial, deep, or opportunistic.
  129. what is candida albicans?
    candida albicans is normally found in the mouth, gastrointestinal tract, and vagina of normal individuals. Changes in pH and use of antibiotics that destroy bacteria that normally inhibit Candida growth permit rapid proliferation and overgrowth, which can lead to superficial or deep infection
  130. what happens when you use too many antibiotics?
    Overuse of antibiotics can lead to the destruction of the normal flora, allowing the selective overgrowth of antibiotic-resistant strains or pathogens that had previously been controlled
  131. what happens if you don't complete your antibiotic regimen?
    Lack of compliance concerning the necessity of completing the therapeutic regimen with antibiotics allows the selective resurgence of microorganisms that are more relatively resistant to the antibiotic
  132. what is an example of destruction of normal flora after using antibiotics often?
    after treatment with the antibiotic clindamycin, the normal intestinal flora can become compromised, allowing the overgrowth of Clostridium difficile and the development of pseudomembranous colitis (a bacterial infection of the intestines)
  133. What are vaccines?
    Vaccines are biologic preparations of weakened or dead pathogens that when administered stimulate production of antibodies or cellular immunity against the pathogen without causing disease
  134. Whats the purpose of vaccination?
    The purpose of vaccination is to induce long-lasting protective immune responses under conditions that will not result in disease in a healthy recipient of the vaccine
  135. Whats the primary immune response from vaccination?
    The primary immune response from vaccination is generally short lived; therefore booster injections are used to push the immune response through multiple secondary responses that result in large numbers of memory cells and sustained protective levels of antibody or T cells, or both
  136. What is an attenuated virus? and why do you use them?
    vaccines against viral infection (measles, mumps, rubella, varicella [chickenpox]) contain live viruses that are weakened (attenuated virus) so they continue to express appropriate antigens but establish only a limited and easily controlled infection
  137. How has the pertussis vaccine changed?
    Pertussis (whooping cough) vaccine has been changed from a killed whole-cell vaccine to cellular extract (acellular) vaccine that contains the pertussis toxoid and additional bacterial antigens
  138. How did the change in the pertussis vaccine help?
    it has dramatically reduced adverse side-effects
  139. What is herd immunity?
    Depending on the microorganism, a certain percentage of the population (usually about 85%) should be immunized in order to achieve protection of the total population.
  140. What is Acquired immunodeficiency syndrome? or AIDS?
    Acquired immunodeficiency syndrome is a secondary immune deficiency that develops in response to viral infection.
  141. What is HIV?
    The human immunodeficiency virus (HIV) infects and destroys the Th cell, which is necessary for the development of both plasma cells and cytotoxic T cells. HIV suppressed immune response against itself
  142. What is the epidemiology of AIDS?
    HIV is a blood-borne pathogen with the typical routes of transmission: blood or blood products, intravenous drug abuse, both heterosexual and homosexual activity, and maternal-child transmission before or during birth.
  143. what is the treatment and prevention of AIDS?
    Approved AIDS medications are classified by mechanism of action: nucleoside and nonnucleoside inhibitors of reverse transcriptase (reverse transcriptase inhibitors), inhibitors of the viral protease (protease inhibitors), inhibitors of cell fusion (cell fusion inhibitors), inhibitors of viral entrance into the target cell (entrance inhibitors), and inhibitors of the viral integrase (integrase inhibitors)
  144. what is hypersensitivity
    Hypersensitivity is an altered immunologic response to an antigen that results in disease or damage to the individual
  145. What is autoimmunity?
    Autoimmunity is a disturbance in the immunologic tolerance of self-antigens.
  146. what is immediate hypersensitivity?
    Reactions that occur within minutes to a few hours after exposure to antigen are termed immediate hypersensitivity reactions.
  147. what are delayed hypersensitivity?
    these reactions may take several hours to appear and are at maximal severity days after reexposure to the antigen.
  148. What is the most rapid immediate hypersensitivity?
    The most rapid and severe immediate hypersensitivity reaction is anaphylaxis
  149. What is Type I: IgE-Mediated Hypersensitivity Reactions?
    Type I reactions are mediated by antigen-specific IgE and the products of tissue mast cells (Figure 7-9). Most common allergic reactions are type I reactions
  150. what are Mechanisms of IgE-mediated hypersensitivity?
    The most potent mediator of IgE-mediated hypersensitivity is histamine, which affects several key target cells.
  151. What are the clinical manifestations of type I rxns?
    are attributable mostly to the biologic effects of histamine. The tissues most commonly affected by type I responses contain large numbers of mast cells and are sensitive to the effects of histamine released from them
  152. What are examples of the tissues most commonly effected by type I rxns?
    These tissues are found in the gastrointestinal tract, the skin, and the respiratory tract
  153. What are the causes of GI allergies?
    Gastrointestinal allergy is caused primarily by allergens that enter through the mouth—usually foods or medicines. Foods most often implicated in gastrointestinal allergies are milk, chocolate, citrus fruits, eggs, wheat, nuts, peanut butter, and fish
  154. Symptoms of GI allergies?
    Symptoms include vomiting, diarrhea, or abdominal pain.
  155. what is the most common GI allergy in adults?
    shellfish allergy and can initiate an anaphylactic
  156. what is urticaria?
    Urticaria, or hives, is a dermal (skin) manifestation of allergic reactions
  157. what are manifestations of allergic rxns as a result of type I hypersensitivity?
    they include pruritus, angioedema (swelling caused by exudation), edema of the larynx, urticaria (hives), bronchospasm (constriction of airways in the lungs), hypotension (low blood pressure), and dysrhythmias (irregular heartbeat) because of anaphylactic shock, and gastrointestinal cramping caused by inflammation of the gastrointestinal mucosa
  158. What are type IV rxns?
    type IV reactions are mediated by T lymphocytes and do not involve antibody
  159. What is a delayed hypersensitivity skin test? an example?
    The reaction follows an intradermal injection of tuberculin antigen into a suitably sensitized individual and is called a delayed hypersensitivity skin test because of its slow onset—24 to 72 hours to reach maximal intensity
  160. what is Development of Allergic Contact Dermatitis?
    • A. The development of allergy to poison ivy.
    • B. Contact dermatitis caused by a delayed hypersensitivity reaction leading to vesicles and scaling at the sites of contact.
  161. what is the most common hypersensitivity disease?
    allergies
  162. what type are the majority of allergies?
    The majority of allergies are type I reactions that lead to annoying symptoms, including rhinitis, sneezing, and other relatively mild reactions. In some individuals, however, these reactions can be excessive and life-threatening (anaphylaxis)
  163. Bee stings and allergies?
    Bee venoms contain a mixture of enzymes and other proteins that may serve as allergens. About 1% of children may have an anaphylactic reaction to bee venom
  164. What are the symptoms like and how long do they take to come about for a bee sting?
    Within minutes they may develop excessive swelling (edema) at the bee sting site, followed by generalized hives, pruritus, and swelling in areas distal from the sting (e.g., eyes, lips), and other systemic symptoms including flushing, sweating, dizziness, and headache
  165. what are the severe symptoms of bee stings?
    The most severe symptoms may include gastrointestinal (e.g., stomach cramps, vomiting), respiratory (e.g., tightness in the throat, wheezing, difficulty breathing), and vascular (e.g., low blood pressure, shock) reactions. Severe respiratory and vascular reactions may lead to death.
  166. What is SLE?
    Systemic lupus erythematosus (SLE) is the most common, complex, and serious of the autoimmune disorders
  167. What are the ABO groups antigens?
    The ABO blood group consists of two major carbohydrate antigens, labeled A and B (Figure 7-15), that are expressed on virtually all cells
  168. A blood type?
    The erythrocytes of persons with blood type A have the type A carbohydrate antigen (i.e., carry the A antigen)
  169. B blood type?
    those with blood type B carry the B antigen
  170. AB blood type?
    those with blood type AB carry both A and B antigens
  171. O blood type?
    • those of blood type O carry neither the A nor the B antigen
    • they are anti-A and anti-B
    • they contain IgM antibodies against both A and B carbohydrates
  172. what are the natural occurring antibodies in the blood called?
    isohemagglutinins, are IgM immunoglobulins and are induced early in life against similar antigens expressed on naturally occurring bacteria in the intestinal tract.
  173. what is the universal donor?
    Type O blood. meaning anyone can accept their blood
  174. What blood type is the universal recipient?
    Type AB because they lack both anti-A and anti-B antibodies
  175. What is Rh system?
    • The Rh blood group is a group of antigens expressed only on red blood cells
    •  Individuals who express the D antigen on their red cells are Rh-positive, whereas individuals who do not express the D antigen are Rh-negative
  176. What is hemolytic disease of the newborn?
    It is when the mom is rH negative and the baby is rH positive. The moms antibodies cross the placenta and destroy the red blood cells of the fetus.
  177. what is RhoGam?
    It is the drug given to the rH neg. mom with an rH positive fetus so problems don't occur
  178. MHC molecules and organ transplants?
    The diversity of MHC molecules becomes clinically relevant during organ transplantation.25 The recipient of a transplant can mount an immune response against the foreign MHC antigens on the donor tissue, resulting in rejection
  179. how do you minimize tissue rejection?
    the donor and recipient are often tissue-typed beforehand to identify differences in HLA antigens.
  180. what are stress-related disorders?
    Americans have become accustomed to an accelerated way of life with chronic stress by adopting behaviors (e.g., smoking, drinking, drug abuse, sleep disturbances) that may result in the so-called stress-related disorders
  181. what are the three stages of GAS?
    (1) the alarm stage or rxn, in which the CNS is aroused and the body's defenses are mobilized (e.g., “fight or flight”)(2) the stage of resistance or adaptation, during which mobilization contributes to “fight or flight;”(3) the stage of exhaustion, where continuous stress causes the progressive breakdown of compensatory mechanisms (acquired adaptations) and homeostasis
  182. What is the alarm rxn?
    The alarm reaction includes increased secretion of glucocorticoids (cortisol) by the adrenal cortex and increased secretion of epinephrine and small amounts of norepinephrine from the adrenal medulla
  183. What is HPA?
    Hypothalamic-Pituitary-Adrenal (HPA) Axis. The response to stress begins in the brain
  184. what does the hypothalamus do?
    The hypothalamus is the control center in the brain for many hormones including corticotropin-releasing hormone (CRH).
  185. What are catecholamines?
    Circulating catecholamines essentially mimic direct sympathetic stimulation. Catecholamines cannot cross the blood-brain barrier and are synthesized locally in the brain.
  186. What are Glucocorticoids: Cortisol?
    During stress ACTH activates the adrenal cortex, increasing secretion of glucocorticoid hormones, primarily cortisol. (Cortisol is known outside the body as hydrocortisone.)

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