Hypersensitivity reactions

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Discusses the four types of hypersensitivity disorders.

Hypersensitivity reactions

  1. 1. What happens when the immune system doesn’t work the way it should?? 1
  2. 2. What makes us sick?  “enemies” in the environment in the form of microbes and chemicals are constantly attacking our bodies, disrupting homeostasis  sometimes immune system homeostasis is disrupted on its ownit may over-react to antigens such as with allergies  it may react to self proteins as with autoimmune disease it may under-react as with human immunodeficiency virus infection (HIV) 2
  3. 3. OVER-REACTION TOANTIGENS
  4. 4. Over-reaction to antigens Pollen grains Mast cell ©Dennis Kunkel Microscopy, Inc., www.DennisKunkel.com•the immune system reacts to antigens (allergens) that don’tcause a reaction in most people – like pollen 4
  5. 5. Over-reaction to antigens a type of antibody called IgE binds to the allergen causing mast cells to produce chemicals called histamines. Common symptoms include:  runny nose and itchy, watery eyes, with repeated exposure resulting in a more rapid onset of symptoms treatments  antihistamines are given to counteract the histamines  shots containing low doses of an allergen can help a person to become desensitized to that specific antigen 5
  6. 6. Disorders of the immune system1. Allergy2. Autoimmune disease3. Immunodeficiency
  7. 7.  The immune system is an integral part of human protection against disease, but the normally protective immune mechanisms can sometimes cause detrimental reactions in the host. Such reactions are known as hypersensitivity reactions, and the study of these is termed immunopathology.
  8. 8.  The traditional classification for hypersensitivity reactions is that of Gell and Coombs and is currently the most commonly known classification system. It divides the hypersensitivity reactions into the following 4 types:
  9. 9.  Type I reactions  Immediate hypersensitivity reactions Type II reactions  Cytotoxic hypersensitivity reactions Type III reactions  Immune-complex reactions Type IV reactions  Delayed hypersensitivity reactions, cell-mediated immunity
  10. 10.  Type I reactions  involve immunoglobulin E (IgE)–mediated release of histamine and other mediators from mast cells and basophils. Type II reactions  involve immunoglobulin G or immunoglobulin M antibodies bound to cell surface antigens, with subsequent complement fixation. Type III reactions  involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation. Type IV reactions  mediated by T cells rather than by antibodies.
  11. 11.  Some authors believe this classification system may be too general and favor a more recent classification system proposed by Sell et al. This system divides immunopathologic responses into the following 7 categories: 1. Inactivation/activation antibody reactions 2. Cytotoxic or cytolytic antibody reactions 3. Immune-complex reactions 4. Allergic reactions 5. T-cell cytotoxic reactions 6. Delayed hypersensitivity reactions 7. Granulomatous reactions
  12. 12. Hypersensitivity reaction undesirable side effect of immunity manifesting trivial discomforts such as itching of the skin to potentially fatal disease such as bronchial asthma. initiated by the interaction of antigen w/ humoral antibody or by cell-mediated immune mechanisms.
  13. 13. Type I. Anaphylactic TypeType II. Cytotoxic TypeType III. Immune Complex-MediatedType IV. Cell-MediatedType V. Stimulatory Reactions
  14. 14. HypersensitivityThere are four different types of hypersensitivities that result from different responses of the immune system:Type I: Immediate hypersensitivity - onset within minutes of antigen challenge - examples are allergies to molds, insect bitesType II: Cytotoxic hypersensitivity - onset within minutes or a few hours of antigen challenge - examples are adult hemolytic anemia and drug allergiesType III: Immune complex-mediated hypersensitivity - onset usually within 2-6 hours - examples include serum sickness and systemic lupus erythematosusType IV: Delayed Hypersensitivity 14 - inflammation by 2-6 hours; peaks by 24-48 hours
  15. 15. Process of Allergy Step 1: Sensitization  Occurs when one develops IgE antibodies against a substance that is inhaled, ingested, or injected  Newly formed IgE antibodies stick to basophils and mast cells no s/s yet Step 2: Reexposure to allergen  (+) s/s  Cellular events for all immediate allergic reactions is the same
  16. 16.  Reexposure to the antigen can then result in the antigen binding to and cross-linking the bound IgE antibodies on the mast cells and basophils. This causes the release and formation of chemical mediators from these cells. These mediators include  preformed mediators,  newly synthesized mediators,  cytokines
  17. 17. Type I:Immediate hypersensitivity
  18. 18. Type I. Immediate Hypersensitivity Reactions rapidly developing immunologic reaction occurring w/in minutes after the combination of an antigen w/ antibody bound to mast cells or basophils in individuals previously sensitized to the antigen. may occur as a systemic or as a local reaction.
  19. 19. Etiology Allergic reactions  Reactions can be elicited by various aeroallergens (eg, pollen, animal dander), drugs, or insect stings.  Other possible causes are latex, drug, and food allergy.
  20. 20. Biological basis allergies histamine
  21. 21. Etiology Allergens  Allergens can be complete protein antigens or low–molecular- weight proteins capable of eliciting an IgE response.  Pollen and animal dander represent complete protein antigens.  Haptens are low–molecular-weight (inorganic) antigens that are not capable of eliciting an allergic response by themselves.  must bind to serum or tissue proteins in order to elicit a response.  a typical cause of drug hypersensitivity reactions.  Note that all drug hypersensitivity reactions are not mediated by IgE.  In addition to anaphylactoid reactions, drug reactions can be caused by cytotoxicity and immune-complex formation and by other immunopathologic mechanisms.
  22. 22. Etiology Foods  most common food allergens are  peanuts, tree nuts, finned fish, shellfish, eggs, milk, soy, and wheat.  Certain foods can cross-react with latex allergens.  These foods include banana, kiwi, chestnut, avocado, pineapple, passion fruit, apricot, and grape.
  23. 23. Etiology Hymenoptera  Bee, wasp, yellow jacket, hornet, and fire ant stings can cause IgE-mediated reactions.  While anaphylaxis is the most serious reaction, localized swelling and inflammation can also occur and do not by themselves indicate increased risk of a subsequent life-threatening reaction.  At least 50 Americans die each year from anaphylaxis caused by a stinging insect.
  24. 24. Systemic reaction usually IV injection of an antigen to which the host has already become sensitized  state of shock can be produced within minutes (may be fatal)
  25. 25. Local reactions depend on the portal of entry of the allergen. May take the form of: localized cutaneous swelling (skin allergy, hives) nasal & conjunctival discharge (allergic rhinitis and conjunctivitis) hay fever bronchial asthma allergic gastroenteritis (food allergy)
  26. 26. Type I hypersensitivity – sensitization to an inhaledallergen or bee sting cytokines   Mast cell Antigens (red dots) from inhaled pollen are ingested and presented by macrophages to T cells. Activated T cells produce cytokines leading to the production of IgE, which binds to receptors on mast cells and causes the release of histamine, which is responsible for allergy symptoms. Onset is usually within minutes of contact with antigen. 27
  27. 27. Initial response •vasodilation •vascular leakage •smooth muscle spasmsAllergens stimulate immune system cells to Late phase reactionmake antibodies and chemical signals (such ashistamine) to induce inflammation •mucosal edema •mucus secretion •leukocyte infiltration •epithelial damage •bronchospasm
  28. 28. Allergy is characterized by a local orsystemic inflammatory response to allergensLocal symptoms: Nose: swelling of the nasal mucosa (allergic rhinitis) Eyes: redness and itching of the conjunctiva (allergic conjunctivitis) Airways: bronchoconstriction, wheezing, sometimes outright attacks of asthma Ears: feeling of fullness, possibly pain, and impaired hearing due to the lack of eustachian tube drainage. Skin: various rashes, such as eczema, hives and contact dermatitis. Head: while not as common, headaches are seen in some with environmental or chemical allergies.Systemic allergic response Is also called anaphylaxis Depending of the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma and even death.
  29. 29. Allergen IgE production by B lymphocytes (at the site of entry of antigen & draining LNs) IgE antibodies attach to mast cells and basophilsThe person is sensitized to that allergen. Memory cells are generated.
  30. 30. Re-exposure to the allergen Binding of allergen to 2 adjacent IgE molecules on the surface of a basophil or mast cell Destortion of the cell membrane causing them to degranulateRelease of vasoactive amines (histamine) into the circulation.
  31. 31. HistamineIncreased capillary Increased mucus Pruritus and permeability secretion erythema Edema, facial Watery nasal and puffiness conjunctival discharge Primary Phase
  32. 32. Secretion of leukotrienes and prostaglandins Stimulation of more WBCGeneralized inflammatory reaction Secondary Phase
  33. 33. DX TESTS
  34. 34. Laboratory• CBC – Increased WBC – eosinophil count• Increased serum IgE levels – Normal values 39IU/ml – Does not determine indicate specific antigen• Radioallergosorbent Test (RAST) – Determines the blood concentration of IgE directed against a specific antigen and thus can determine specific antigen
  35. 35. Allergy testing Scratch test Intradermal test Oral food challenge In vitro testing
  36. 36. Allergy Testing Skin Testing  Scratch Test  Results in an immediate hypersensitivity reaction to an allergen  Discontinue antihistamines for 5 days before the test  Allergens are introduced through a superficial scratch or prick cause a localized reaction (wheal) when the test result is positive  Serious reactions are rare
  37. 37. Skin test The allergens are either injected intradermally or into small scratchings made into the patients skin If the patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes. This response will range from slight reddening of the skin to full-blown hives in extremely sensitive patients. Problems: some people may display a delayed-type hypersensitivity (DTH) reaction which can occur as far as 6 hours after application of the allergen and last up to 24 hours. This can also cause serious long-lasting tissue damage to the affected area. These types of serious reactions are quite rare.
  38. 38.  Wash the solution from the skin Topical steroids and oral antihistamines are administered to reduce itching ( sedation)
  39. 39.  Intradermal Testing  Reserved for substances that are strongly suspected of causing allergy but did not test positive during scratch test  Greater risk for anaphylaxis occurs
  40. 40.  Oral Food Challenge  Effective for some individuals in identifying specific allergens when skin testing has been inconclusive  Eliminate suspected foods for 7-14 days before testing  Eat a defined food for at least one day and monitor clients reaction
  41. 41. In Vitro Testing • Drawing blood from a client and exposing it to different panels containing food and mold allergens • After incubation the cells are checked • Positive reaction – Increase WBC size by 12 % – Increased platelet aggregation
  42. 42. COLLABORATIVEMANAGEMENT
  43. 43. Collaborative Management• Avoidance Therapy
  44. 44. Medications Decongestants  vasoconstriction in the inflamed tissue thereby reducing the edema  Caution in patients with HPN, glaucoma Antihistamines  blocks histamine from binding with its receptor preventing vasodilation and capillary permeability  Sedation
  45. 45.  Corticosteroids  decrease inflammation by preventing the synthesis of mediators  Nasal  Beclomethasone  Fluticasone  Oral  Prednisolone  Prednisone
  46. 46.  Mast Cell Stabilizers  Prevent mast cell membranes from opening when allergen binds to IgE  Cromolyn sodium Leukotriene Inhibitors  Zileuton  Zafirlukast
  47. 47. Desensitization The most common form of desensitization involves subcutaneous injections of small amount of the allergen An increasing dose is usually given weekly until the patient is receiving a 0.5ml dose Recommended course of treatment is approximately 5 years
  48. 48. Desensitization The mechanism of action to reduce allergic responses by desensitization is thought to be competition. Instead of IgE , IgG is produced and binds with the allergens so as not to cause degranulation of mast cells or basophils.
  49. 49.  Desensitization has been effective for a few antigens, particularly bee venom. This type of treatment is designed to cause an IgG response instead of an IgE response. The allergen is either ingested or injected into the subject starting in small amounts and increased to larger amounts. This treatment can have 2 effects: T-helper 1 cells produce more IgG which binds to the antigen so that it can’t bind to IgE receptors on mast cells and cause release of histamines. 2) IgG binds to and removes the antigen before it binds to T-helper 2 cells. The T- helper 2 cells will then not be able to produce the B cells that will produce IgE.
  50. 50. ALLERGIC RHINITIS
  51. 51. Allergic rhinoconjunctivitis s/s Congestion Sneezing Itchy , runny nose and eyes; Itching of the palate and inner ear. postnasal drip, which can cause sore throat, coughing, or throat clearing.
  52. 52. Rhinoconjunctivitis usually results from exposure to aeroallergens can be seasonal or perennial. Airborne allergens typically also cause ocular symptoms consisting of itchy eyes, tearing, swelling or redness of the eyes. Repeated exposure to the allergen can result in chronic allergic inflammation, which causes chronic nasal congestion that can be further complicated by sinusitis.
  53. 53. s/s Patients may sneeze, be congested, have a runny nose, or have frequent throat clearing and/or cough from postnasal drip. Sclera may be injected, and patients may have dark rings under the eyes (ie, allergic shiners). Nasal mucosa can be boggy and pale, usually with clear drainage. The pharynx may have a cobblestone appearance reflecting lymphoid hyperplasia from postnasal mucus drainage. The patient may have frontal or maxillary sinus tenderness from chronic sinus congestion or infection.
  54. 54. allergic shiners
  55. 55. Additional Diagnostic test Nasal smear tests  look for eosinophils.  However, regular use of a nasal corticosteroid can lower the eosinophil count.  Elevated eosinophil levels can be consistent with allergic rhinitis.
  56. 56. Mgmt Avoid the offending allergen, if possible. Oral H1-receptor blockers  helpful for controlling itchiness, rhinorrhea, and lacrimation but most have little effect on nasal congestion. intranasal glucocorticosteroid  control nasal symptoms, including nasal congestion.  need to be used regularly to be effective  patients may need to use them for a week or more before maximum effect is seen.
  57. 57. Mgmt Other topical nasal agents include  azelastine  olopatadine (H1-receptor blockers)  cromolyn (a mast cell stabilizer). Nasal antihistamines have a rapid onset of action and can be used on an as-needed basis.
  58. 58. Mgmt Topical nasal decongestants can provide immediate relief of nasal congestion and can be used temporarily and as needed. Note: Patients should be cautioned not to use them for more than a few days, however, as they can cause rebound congestion (rhinitis medicamentosa).
  59. 59. Mgmt ocular symptoms  Topical decongestants, mast cell stabilizers, or antihistamines  artificial tears - can be refrigerated for an extra cooling effect.  Cold compresses can also be used. Note: use of topical decongestants should be limited to a few days, as longer use can result in rebound vasodilation.
  60. 60. Antigen-injection immunotherapy AKA: subcutaneous immunotherapy (SCIT) very effective in treating inhalant allergies and can be considered in patients whose symptoms do not respond well to medications or in patients who cannot avoid the allergen in question (eg, cat owner allergic to cats). The mechanism of action of immunotherapy is not yet fully elucidated.
  61. 61. Sublingual/swallow immunotherapy (SLIT) An alternative to antigen-injection immunotherapy currently being used with increasing frequency in Europe. involves having the patient hold extract under the tongue for 1-3 minutes before swallowing. It offers the advantage of a lower likelihood of systemic adverse effects and has been shown to reduce allergic rhinitis and asthma symptoms. may have a more significant impact on these symptoms than SLIT. still being evaluated for FDA approval in the United States.
  62. 62. ASTHMA
  63. 63. Allergic asthma s/s Bronchoconstriction shortness of breath (eg, difficulty getting air out), wheezing, cough, and/or chest tightness. Long-term allergen exposure can cause  chronic changes of increased difficulty breathing and  chest tightness  and the patient may give a history of repeated rescue inhaler use or reduced peak flows.
  64. 64.  Patients may be coughing or appear short of breath. Wheezing may be present, but it might not be heard in patients with milder symptoms or, if the asthma is very severe, patients may not move enough air to produce wheezing. Breaths may be shallow or the patient may have a prolonged expiratory phase. Cyanosis of the lips, fingers, or toes (caused by hypoxemia) may occur with severe asthma.
  65. 65. Additional diagnostic tests Spirometry/pulmonary function tests  Spirometry or pulmonary function tests offer an objective means of assessing asthma.  Peak-flow meters can also be used for this and can be used by patients at home to monitor their status. Inhalation challenge with histamine, methacholine, and specific allergen  confirm airway hypersensitivity or allergen sensitivity. Measurement of exhaled nitric oxide  used to evaluate inflammation in the airways seen with asthma and to follow efficacy of or adherence to anti-inflammatory medications (eg, inhaled corticosteroids). Induced sputum:  Sputum induced from the airways can be evaluated for eosinophils, which is a measure of inflammation seen in asthma.
  66. 66. Mgmt Avoid the offending allergen, if possible. A key factor in controlling allergic asthma is controlling allergic rhinitis symptoms.
  67. 67. Mgmt Therapy depends on the severity of disease. albuterol metered-dose inhaler (MDI) (or nebulizers for young children) to use as needed. Inhaled glucocorticosteroids should be added if appropriate. In general, these medications are used if symptoms occur more than twice weekly or if abnormal spirometry findings reverse with the inhalation of a short-acting bronchodilator. .
  68. 68. Mgmt For more refractory symptoms  long-acting beta agonist may be added to the inhaled glucocorticoid Leukotriene inhibitors can also be added. Systemic corticosteroid bursts may need to be used for exacerbations of severe cases. Patients with allergic asthma may respond well to specific allergen immunotherapy.
  69. 69. Mgmt omalizumab (Xolair)  a humanized monoclonal antibody that prevents binding of IgE to high-affinity IgE receptors on mast cells and basophils  In patients refractory to the usual medications and who have antigen-specific IgE to perennial environmental aeroallergens (positive skin test or RAST result)
  70. 70. URTICARIA / ANGIOEDEMA
  71. 71. Urticaria/angioedema s/s Diffuse hives or wheals may occur and cause significant pruritus; individual wheals resolve after minutes to hours, but new wheals can continue to form. Acute urticaria (lasting < 6 wk) can be caused by viral infections, foods, drugs, or contact allergens. Chronic urticaria lasts longer than 6 weeks. Although many causes are possible, often, a cause is not found. In many cases, this is not due to antigen-IgE – mediated immediate hypersensitivity but to an autoantibody to the high affinity IgE receptor or to IgE itself.
  72. 72.  (+) wheals with surrounding erythema.  Wheals from allergic causes usually last a few minutes to a few hours.  Wheals due to cutaneous vasculitis may last more than 24 hours and may leave postinflammatory hyperpigmentation upon healing.
  73. 73.  Angioedema  is localized tissue swelling that can occur in soft tissues throughout the body.  pain at the site of swelling instead of pruritus, which occurs with urticaria.  particularly concerning if pharyngeal or laryngeal tissues are involved. Angioedema of the laryngopharynx  can obstruct the airway; difficulty breathing.  Stridor or hoarseness  can be life threatening.
  74. 74. Mgmt Avoid the offending allergen if known. H1-receptor blocker should be added.  If symptoms are not controlled with this alone,  an H2-receptor blocker, leukotriene inhibitor, or oral glucocorticosteroid can be added.  Most patients require higher than the usual doses;  employing twice daily H1 and H2 antihistamines for successful control is not uncommon.
  75. 75. ATOPIC DERMATITIS
  76. 76. Atopic dermatitis is an eczematous cutaneous eruption more common in children than in adults; can be exacerbated by allergen exposure, especially food allergies (+) pruritus which produces the lesions.  Superinfection with staphylococcal organisms can occur, particularly in severely excoriated or cracked lesions.
  77. 77.  physical examination findings can vary with the severity of the disease.  less severe cases - skin can appear normal, dry, or with erythematous papules.  more severe cases - patients can have extremely dry, lichenified, cracked, and, sometimes, crusted lesions. In infants, the head and extensor surfaces are more involved, whereas in older children and adults, the flexural surfaces tend to be affected.
  78. 78. Mgmt Avoid the offending allergen if possible, and properly hydrate and care for the skin. Topical glucocorticosteroids and topical immunomodulators (eg, tacrolimus) can be used.
  79. 79. ANAPHYLAXIS
  80. 80. Anaphylaxis Most dramatic and life-threatening Occurs rapidly and systematically Affects many organs within seconds to minutes after allergen exposure Not common Fatal
  81. 81. s/s Generalized pruritus and urticaria Erythema and angioedema Bronchoconstriction, mucosal edema and excess mucus production Wheezes , crackles Anaphylactic shock
  82. 82.  Vital signs should be monitored closely because patients can quickly progress to circulatory and/or respiratory failure. Tachycardia may precede hypotension. Patients who are hypotensive may have reflex tachycardia, but bradycardia can also occur in 5%. Patients may have urticaria, angioedema, or both. Angioedema of the airway and throat can result in respiratory failure or asphyxiation; therefore, this dangerous occurrence must be closely monitored. Patients may be wheezing during the respiratory examination, which is secondary to bronchoconstriction. Confusion and alteration of mental status can occur.
  83. 83. Collaborative Management Establish and maintain airway High fowlers position Apply tourniquet immediately proximal to the allergen point of entry when possible O2 by mask Assess the level of consciousness and vital signs.
  84. 84.  Administer medications as ordered  Epinephrine 0.3-.05ml subq  Antihistamines – diphenhydramine IM or IV  Aminophylline – theophylline IV for severe bronchospasm  Corticosteriods – hydrocortisone, solumedrol IV  B2 agonists nebulization – Salbutamol, terbutaline,
  85. 85.  Administer epinephrine immediately Start intravenous fluids: Plain NSS or LR  should be administered rapidly and as blood pressure and overall fluid status warrant. Consider other vasopressors (eg, dopamine) if hypotension does not respond to the above measures. Norepinephrine may be used if dopamine is not effective.
  86. 86. Epipen
  87. 87.  isoproterenol should not be used  because it is a peripheral vasodilator. Patients with beta-adrenergic blockade may be particularly difficult to treat.  They have both chronotropic and inotropic cardiac suppression and may not respond to the above treatments.  Glucagon has positive inotropic and chronotropic effects and is the drug of choice in these cases.  Atropine can also be used but will only be effective in treating bradycardia.
  88. 88.  H1- and H2-receptor blockers  can be helpful in alleviating hypotension, pruritus, urticaria, rhinorrhea, and other symptoms.  Cimetidine, when combined with any of several H1 antihistamines, has been demonstrated to block histamine-induced hypotension. Use albuterol nebulizers if needed. Administer a corticosteroid, which is believed to help prevent or control the late-phase reaction.
  89. 89. Late phase reactions Transfer the patient to the hospital for further observation and care. Late phase reactions  can occur 4-6 hours after the initial reaction  can be as severe as or worse than the original reaction.  In some cases, can occur up to 36 hours later.  Education of the patient and observation is, therefore, important. http://emedicine.medscape.com/article/136217-treatment#showall
  90. 90. Prevention Avoid the triggering allergen as much as possible. Patients should be given a prescription for at least 2 autoinjectable epinephrine doses (eg, 2 EpiPens or 1 Twinject) and instructed in their proper use. Importantly, patients must carry them at all times. Patients can also be instructed to carry both an H1 and an H2 antihistamine with them.
  91. 91.  Patients must wear a Medic Alert type of bracelet to alert emergency responders to the possibility of anaphylaxis. Patients should be taught what measures to take in case of a future anaphylactic reaction  e.g., immediately administer epinephrine and take the antihistamine,  call emergency services (eg, 911),  or go to the nearest emergency department (even if feeling better after the epinephrine).
  92. 92.  Specific allergen immunotherapy is highly effective in preventing anaphylaxis from hymenoptera stings and should always be considered for patients who have experienced a systemic reaction after an insect sting. http://emedicine.medscape.com/article/136217-treatment#showall
  93. 93. Anaphylactoid reactions Non–IgE-mediated mast cell and basophil degranulation can occur from a variety of substances. Although the mechanisms are different, the clinical manifestations can appear the same. Causes can include  radiocontrast dye, opiates, and vancomycin (eg, red man syndrome).
  94. 94. Anaphylactoid reactions Mgmt glucocorticosteroids and both H1 and H2 antihistamines  Pretreatment prior to exposure to iodinated radiocontrast dye  this, together with the use of low-osmolal nonionic dye, reduces the risk of a repeat reaction to approximately 1%. Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs)  can also cause reactions by causing release of leukotrienes  Patients susceptible to this syndrome can develop acute asthma exacerbation, nasal congestion, urticaria, or angioedema after ingestion.
  95. 95. LATEX ALLERGY
  96. 96.  Protein found in processed natural latex rubber products
  97. 97. Latex Allergy
  98. 98.  Avoid products containing latex (surgical gloves, tubings, condoms etc.) Other interventions similar to hypersensitivity reactions
  99. 99.  Use synthetic substances that do not contain latex protein ElastyLite gloves; other tubings, etc
  100. 100. GI ALLERGIES
  101. 101. GI allergies s/s Patients may report nausea, vomiting, abdominal cramping, and diarrhea after ingestion of the offending food. Note that other mechanisms (eg, lactose intolerance) commonly cause these symptoms. Eosinophilic esophagitis and gastritis are newly recognized syndromes that may be allergic in nature.
  102. 102. Type II:Cytotoxic hypersensitivity
  103. 103. Type II. Cytotoxic Type Body makes special autoantibodies directed against self-cells (antigens present on the surface of cells or other tissue components) antigen:  1. may be intrinsic to the cell membrane  2. may take the form of an exogenous antigen adsorbed on the cell surface. hypersensitivity results from the binding of antibodies to normal or altered cell-surface antigens
  104. 104. Type II examples1. Transfusion reactions  cells from an incompatible donor react w/ the host’s antibody2. Erythroblastosis fetalis  there is an antigenic difference between the mother & the fetus, and antibodies (IgG) cross the placenta & cause destruction of fetal red cells.3. Autoimmune hemolytic anemia, agranulocytosis, throbocytopenia  individuals produce antibodies to their own blood cells, w/c are then destroyed. 4. Drug reactions  antibodies are produced that react w/ the drug.
  105. 105. Type II hypersensitivity – immune-mediateddestruction of red blood cells Drug (p=penicillin) modified red blood cells induce the production of antibodies, because the bound drug makes them look foreign to the immune system. When these antibodies are bound to them, the red blood cells are more susceptible to lysis or phagocytosis. Onset is dependent on the presence of specific antibodies.
  106. 106. Maternal antibody formationpreceding sensitization of the fetus to Rh antigen.
  107. 107. Collaborative Management Discontinue the offending agent Plasmapheresis  Filtration of the plasma to remove specific substances like autoantibodies Symptomatic Treatment
  108. 108. RH INCOMPATIBILITY
  109. 109. Rh incompatibility Rh incompatibility occurs when the mothers blood type is Rh negative and her fetus blood type is Rh positive.
  110. 110.  If some of the fetus blood passes into the mothers blood stream, her body will produce antibodies in response.
  111. 111.  these antibodies could pass back through the placenta and harm the fetus red blood cells, causing mild to serious anemia in the fetus. http://www.nationwidechildrens.org/rh-incompatibility
  112. 112. Symptoms Rh incompatibility can cause symptoms ranging from very mild to deadly. In its mildest form, Rh incompatibility causes the destruction of red blood cells. After birth, the infant may have:  Yellowing of the skin and whites of the eyes (jaundice)  Low muscle tone (hypotonia) and lethargy
  113. 113. Complications Possible complications include:  Brain damage due to high levels of bilirubin (kernicterus)  Fluid buildup and swelling in the baby (hydrops fetalis)  Problems with mental function, movement, hearing, speech, and seizures
  114. 114. Signs and tests polyhydramnios A positive direct Coombs test result Higher-than-normal levels of bilirubin in the babys umbilical cord blood Signs of red blood cell destruction in the infants blood
  115. 115. Treatment Because Rh incompatibility is preventable with the use of RhoGAM, prevention remains the best treatment. Treatment of an infant who is already affected depends on the severity of the condition. Infants with mild Rh incompatibility may be treated with:  Feeding and fluids (hydration)  Phototherapy using bilirubin lights
  116. 116. Prevention Rh incompatibility is almost completely preventable. Rh-negative mothers should be followed closely by their obstetricians during pregnancy. Special immune globulins, called RhoGAM, are now used to prevent RH incompatibility in mothers who are Rh-negative. If the father of the infant is Rh-positive or if his blood type cannot be confirmed, the mother is given an injection of RhoGAM during the second trimester. If the baby is Rh- positive, the mother will get a second injection within a few days after delivery.
  117. 117. Prevention These injections prevent the development of antibodies against Rh-positive blood. However, women with Rh-negative blood type must receive injections:  During every pregnancy  If they have a miscarriage or abortion  After prenatal tests such as amniocentesis and chorionic villus biopsy  After injury to the abdomen during pregnancyhttp://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002567/
  118. 118. ABO INCOMPATIBILITY
  119. 119. Symptoms The following are symptoms of ABO incompatible transfusion reactions:  Back pain  Hematuria  Feeling of "impending doom"  Fever  jaundice
  120. 120. Signs and tests The health care provider will perform a physical exam. Blood tests will usually show: Increased Bilirubin level CBC shows damaged to red blood cells or anemia The patients and donors blood are not compatible
  121. 121. Treatment Treatment may include: Antihistamines Steroids IVF Vasopressors http://www.ncbi.nlm.nih.gov/pubmedhealth/ PMH0002283/
  122. 122. Expectations (prognosis) ABO incompatibility can be a very serious problem that can even result in death. With the right treatment, a full recovery is likely. Complications  Kidney failure  Hypotension  Death
  123. 123. Type III: Immune complex- mediated hypersensitivity
  124. 124. Type III hypersensitivity Involve reactions against soluble antigens circulating in serum. Usually involve IgM, IgG antibodies. Antibody-Antigen immune complexes are deposited in organs, activate complement, and cause inflammatory damage.  Glomerulonephritis: Inflammatory kidney damage. Occurs with slightly high antigen-antibody ratio is present.
  125. 125. Type III hypersensitivity – immune complex formation and deposition Immune complexes activate complementImmune complexes of (green dots- C3a, C4a, Inflammation andantigen (red dots) and and C5a), and mast cells edema occur, andantibody form in (yellow cell) degranulate. organ is damagedtarget organ 134
  126. 126.  Every time an antibody binds to antigen, an immune complex is formed. Under normal conditions complexes are bound by complement to RBCs and then eliminated by phagocytes. Complement may also weaken the antibody- antigen bonds thereby re-dissolving the complexes.
  127. 127.  In Type III hypersensitivity, immune complexes are not cleared out and they become deposited in tissues. Immune-complex disease may result from: a) persistent low-grade infection, as in malaria and viral hepatitis; b) autoimmunity, as in rheumatoid arthritis and systemic lupus erythematosis; and c) inhaled antigens, as in farmer’s lung and pigeon fancier’s lung where there is repeated exposure to mold or pigeon antigen.
  128. 128.  In Type III hypersensitivity, the antibody involved is primarily IgG. In the diagram, the presence of immune complexes activates complement (C3a, C4a and C5a are the names given to some of the components of complement), leading to degranulation of mast cells. The products of mast cell degranulation cause blood vessels to become more permeable. This allows immune complexes to be deposited in the walls of blood vessels. Platelets aggregate in the vicinity of the deposits. Neutrophils are attracted to the site but are unable to ingest the complexes because they are bound to the vessel wall. The neutrophils release lysosomal enzymes into the area, causing further damage to the vessel wall.
  129. 129. Type III hypersensitivity – immune complexformation and deposition In sensitized individuals, allergen (antigen) combined with antibody leads to the formation of immune complexes, which activate complement and the inflammatory response. The location of the inflammation depends on the location of the antigen - inhaled, under skin, systemic. Onset is usually within 2-6 hours. 138
  130. 130.  induced by antigen-antibody complexes having the capacity to activate a variety of serum mediators, principally the complement system. Generalized  if immune complexes are formed in the circulation & are deposited in many organ Localized to particular organs:  kidney (glomerulonephritis), joints (arthritis),  small blood vessels of the skin if the complexes are formed and deposited locally (local Arthus reaction)
  131. 131. Arthus reaction• A dermal inflammatory reaction produced under conditions of antibody excess, when a second injection of antigen produces intravascular antigen-antibody complexes which bind complement, causing cell clumping, endothelial damage, and vascular necrosis
  132. 132.  Note: wherever complexes deposit, the tissue damage is the same: complement cascade and the elaboration of biologically active fragments.
  133. 133.  Rheumatoid arthritis Systemic Lupus Erythematosus Serum sickness
  134. 134. SERUM SICKNESS
  135. 135. Serum sickness a condition that may develop when a patient is injected with a large amount of e.g. antitoxin that was produced in an animal or other drugs After about 10 days, anti-antitoxin antibodies react with the antitoxin forming immune complexes that deposit in tissues, walls of the blood vessels, skin, joints, kidney Most common cause is penicillin and animal serum antitoxins
  136. 136. s/s Fever Arthralgia Rash Lymphadenopathy Malaise Polyarthritis and nephritis
  137. 137. Collaborative Management Usually Self limiting Symptomatic treatment  Aspirin for pain  Antihistimines for pruritus  Steroids - prednisone
  138. 138. Type IV: Delayed Hypersensitivity
  139. 139. Type IV hypersensitivity the only type that is not antibody-mediated.  contact hypersensitivity (poison ivy, reactions to metals in jewelry);  tuberculin-type hypersensitivity (the tuberculosis skin test);  granulomatous hypersensitivity (leprosy, tuberculosis, schistosomiasis and Crohn’s disease).
  140. 140.  It is called delayed because its onset may vary;  Occurs hours to days  the length of the delay varies from 72 hours in contact and tuberculin-type to 21-28 days in granulomatous hypersensitivity. Self limiting
  141. 141. Type IV. Cell-Mediated Initiated by specifically sensitized T lymphocytes which respond to an antigen by producing and releasing certain lymphokines and they recruit, retain and activate macrophages to destroy the antigen Antibodies and complement are not involved
  142. 142. Type IV hypersensitivity – delayed-type or contact T cells (blue cells) that recognize Antigen (red dots) antigen are Inflammatory are processed by activated and response causes local APCs release cytokines tissue injury. 155
  143. 143. Type IV hypersensitivity – delayed-type or contact T cells (blue cells) that recognize Antigen (red dots) antigen are Inflammatory are processed by activated and response causes local APCs release cytokines tissue injury. Antigen is presented by APCs to antigen-specific memory T cells that become activated and produce chemicals that cause inflammatory cells to move into the area, leading to tissue injury. Inflammation by 2- 6 hours; peaks by 24-48 hours. 156
  144. 144. Type IV hypersensitivity antigen presented by APCs activates antigen- specific memory T cells (which have been sensitized by prior exposure), causing them to release cytokines that activate and attract other T cells and phagocytic cells to the area. Where the source of antigen is at the skin surface, the APC migrates from the dermis, through lymphatic vessels to a lymph node in order to present antigen to a T cell.
  145. 145.  In the TB skin test, a small amount of soluble antigen (tuberculin) is injected into the skin. The T cells that are activated by the antigen secrete cytokines that draw other cells to the site. Within four hours, neutrophils have arrived, followed by an influx of monocytes and T cells at about 12 hours. The peak of activity is at about 48-72 hours, at which point the area has become red and swollen.
  146. 146. 1. Tuberculin reaction - the best known example of delayed-type hypersensitivity - produced by intracutaneous injection of tuberculin - In previously sensitized individual: reddening and induration of the site(8-12 hours), peaks in 24-72 hours, and thereafter slowly subside.
  147. 147. 2. Transplant rejection3. Contact dermatitis4. Poison Ivy skin rashes5. Local response to insect stings
  148. 148. Patch Testing• Used to identify the allergen• Skin contact with substances to which the client is potentially allergic• Contact with a specific allergen results in a delayed reaction that develops in 48- 96 hours• Substances applied under occlusive tapes• Localized erythema, blister, swelling
  149. 149. Collaborative Management Removal of the offending antigen Monitor reaction site and sites distal to the reaction for circulation adequacy Antihistamines – minimal benefit Steroids
  150. 150. TYPE V. STIMULATORYREACTIONS
  151. 151. Type V. Stimulatory Reactions• Inappropriate stimulation of a normal cell surface receptor by an autoantibody, resulting in an continuous “turned-on” state for the cell• Example – Graves Disease – An autoantibody binds to TSH receptor sites in the thyroid gland stimulating it to produce thyroid hormones continually
  152. 152. Collaborative Management If one organ is involved like in Graves disease ,surgical removal or radiation can be done If more than one organ is involved then immunosuppresion is warranted
  153. 153. THE IMMUNE SYSTEM IN HEALTH AND DISEASE How does your everyday life affect your immune system? 167
  154. 154. Exercise and stress exercise has been shown to boost the immune response  moderate exercise increases the immune response in all age groups  intensive exercise can stress the immune system lack of sleep and exhaustion decrease immune function psychological stress has also been found to decrease immune function 168
  155. 155. Diet a well-balanced diet is essential for good immune system health  fats are very important in the production of WBCs, cytokines and natural killer cells  selenium, zinc, and copper are required in small amounts, which you get if you eat a balanced diet  vitamin E has been shown to boost antibody production in the elderly  vitamin B6 aids in antibody synthesis but mega-dosing can be harmful, too! 169
  156. 156. EnvironmentExposure to certain things in their environment mayactivate the immune systems of some people • Chemicals • Viruses – dioxin – pesticides – solvents • Bacteria • Sunlight • Medication • Food 170
  157. 157. Gender and the immune system women respond to antigens more strongly than men estrogen may affect the development or function of immune cells may explain why more women develop autoimmune diseases 171
  158. 158. SARCOIDOSIS
  159. 159. Sarcoid - close-up of the skin lesions• Sarcoid - close-up of the skin lesions: 20 to 25 percent of individuals with sarcoidosis have skin manifestations as seen in this picture.• The extent of the skin manifestations is difficult to predict, but the most common are red papules that are translucent as seen here.
  160. 160. Erythema nodosum associated with sarcoidosis• This picture shows reddish- purple, hard (indurated), painful nodules (Erythema nodosum) that occur most commonly on the shins. These lesions may be anywhere on the body and may be associated with tuberculosis (TB), sarcoidosis, coccidioidomycosis, systemic lupus erythematosis (SLE), fungal infections, or in response to medications
  161. 161. Sarcoidosis - close-up • Typical sarcoid lesions consist of red, raised lesions (papules) and patches (plaques) with minimal surrounding skin change.
  162. 162. Sarcoidosis on the elbow • These lesions of sarcoidosis are located on the elbow and are red, elevated patches (plaques). The cause of sarcoidosis remains unknown.
  163. 163. Sarcoidosis on the nose and forehead • These are sarcoid lesions on the face. These lesions often appear in scars, as is seen in this photograph.•http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001140/
  164. 164. Sarcoid, stage I - chest x-ray• Sarcoid is primarily a lung (pulmonary) disease. In the early stages, a chest film may show enlargement of lymph nodes in the center of the chest near the heart (mediastinum).
  165. 165. Sarcoid, stage II - chest x-ray• Sarcoid causes damage to the lung tissue that heals by scarring. The film shows a diffuse milky and granular appearance in the normally dark lung areas. This individual has marked decrease in lung function.
  166. 166. Sarcoid, stage IV - chest x-ray• This film shows advanced sarcoid, scarring of the lungs (the light streaking), and cavity formation (the dark areas in the upper right side of the picture).

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