an extreme, often life-threatening allergic reaction to an antigen to which the body has become hypersensitive.,an extreme, often life-threatening allergic reaction to an antigen to which the body has become hypersensitive.
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Added: May 01, 2018
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BY: AJITH PRASAD JOSEPH NIMMY ANN SHIBU ANAPHYLAcTIC SHOCK
DEFINITION Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen. Anaphylaxis is an acute allergic reaction to an antigen (e.g. a bee sting) to which the body has become hypersensitive .
BACKGROUND The term Anaphylaxis is derived from the Greek words ana - (“up, back, again”) and phylaxis (“guarding, protection, immunity”). Anaphylaxis is an acute, potentially fatal, multi organ system reaction caused by the release of chemical mediators from mast cells and basophils. The classic form involves prior sensitization to an allergen with later re-exposure, producing symptoms via an immunologic mechanism. The most common organ systems involved include the cutaneous, respiratory, cardiovascular, and gastrointestinal systems. The full-blown syndrome includes urticaria (hives) and/or angioedema with hypotension and bronchospasm.
PATHOPHYSIOLOGY The traditional nomenclature for anaphylaxis reserves the term anaphylactic for reactions mediated by immunoglobulin E ( IgE ) and the term anaphylactoid for non- IgE -mediated reactions, which can be clinically indistinguishable. There are two types of anaphylaxis : Immunologic : In the immunologic mechanism, immunoglobulin E ( IgE ) binds to the antigen (the foreign material that provokes the allergic reaction). Antigen-bound IgE then activates FcεRI receptors on mast cells and basophils. This leads to the release of inflammatory mediators such as histamine. These mediators subsequently increase the contraction of bronchial smooth muscles, trigger vasodilation, increase the leakage of fluid from blood vessels, and cause heart muscle depression . There is also an immunologic mechanism that does not rely on IgE , but it is not known if this occurs in humans.
PATHOPHYSIOLOGY Non-immunologic : Non-immunologic mechanisms involve substances that directly cause the degranulation of mast cells and basophils. These include agents such as contrast medium, opioids, temperature (hot or cold), and vibration. Sulfites may cause reactions by both immunologic and non-immunologic mechanisms.
PATHOPHYSIOLOGY Anaphylaxis arise from the activation of mast cells and basophils generally involving crosslinking of IgE and aggregation of the high affinity receptors. Upon activation , mast cells and / or basophils quickly release preformed mediators from secretory granules like histamine , tryptase , carboxypeptidase A, and proteoglycans . Downstream activation of phospholipase A2, followed by cyclo-oxygenases and lipo-oxygenases produces arachidonic acid metabolites such as prostaglandins , leukotrienes , and platelet activating factor.
PATHOPHYSIOLOGY The inflammatory cytokines, tumor necrosis factor - is released as a preformed mediator, and also as a late- phase mediator with other cytokines and chemokines .
ETIOLOGY Food : exposure to peanuts, wheat, nuts , certain types of seafood like shellfish, milk, and eggs are the most prevalent causes . Sesame is common in the Middle East, while rice and chickpeas are frequently encountered as sources of anaphylaxis in Asia. Medication : The most common are β-lactam antibiotics (such as penicillin ) followed by aspirin and NSAIDs . Other relatively common causes include chemotherapy, vaccines, protamine and herbal preparations. Some medications ( vancomycin , morphine, x-ray ) cause anaphylaxis by directly triggering mast cell degranulation. Venom : Venom from stinging or biting insects such as Hymenoptera (ants, bees, and wasps) or Triatominae (kissing bugs) may cause anaphylaxis in susceptible people .
DIAGNOSIS The diagnosis of anaphylaxis is based on symptoms that occur suddenly after exposure to the allergen Differential diagnosis Severe asthma Heart attack Panic attack Food poisoning An increased level of histamine and trypt ase can be measured in blood samples during the first three hours after anaphylaxis symptom has begun Tryptase levels are seldom high in food induced anaphylaxis
MANAGEMENT
TREATMENT The primary drug treatments for acute anaphylactic reactions are epinephrine and H1 antihistamines. Medications used in patients with anaphylaxis include the following: Adrenergic agonist s ( eg , epinephrine ) Antihistamines ( eg , diphenhydramine, hydroxyzine ) H2 receptor antagonists ( eg , cimetidine, ranitidine, famotidine) Bronchodilators ( eg , albuterol) Corticosteroids ( eg , methylprednisolone, prednisone ) Positive inotropic agents ( eg , glucagon) Vasopressors ( eg , dopamine
PREVENTION Avoid the responsible allergen Keep an adrenaline kit ( Epipen ) and Benadryl on hand at all times Wear medic alert braclets Venom immunotherapy is highly effective in protecting insect allergic individua ls