Hypersensitivity PDF

Introduction to Hypersensitivity Hypersensitivity is an exaggerated immunologic response, or overreaction, to a foreign antigen or autoimmunity (i.e., a physiological response against an endogenous "self"-antigen). This overreaction is a form of protection to alert the body to an actual or potentia...

Introduction to Hypersensitivity Hypersensitivity is an exaggerated immunologic response, or overreaction, to a foreign antigen or autoimmunity (i.e., a physiological response against an endogenous "self"-antigen). This overreaction is a form of protection to alert the body to an actual or potential health problem. Hypersensitivity reactions are not due to antigens directly but from the inflammatory processes generated by antibodies, immune complexes, or cell-mediated responses. This learning module focuses on the disease processes associated with hypersensitivity and enables you to meet the following course outcomes: CO 1: Analyze pathophysiologic mechanisms associated with selected disease states across the lifespan. CO 2: Examine the way in which homeostatic, adaptive, and compensatory physiological mechanisms can be supported and/or altered through specific therapeutic interventions across the lifespan. CO 3: Distinguish risk factors associated with selected disease states across the lifespan. CO 4: Integrate advanced pathophysiological concepts in the diagnosis and treatment of health problems in selected populations. Symptoms of Hypersensitivity Reaction In a primary care office, a nurse practitioner (NP) assesses a client who reports taking a new medication 30 minutes before arrival. The NP is concerned that the client may be having a hypersensitivity reaction. Which clinical manifestations should the NP expect from the column on the left? Drag and drop expected symptoms of hypersensitivity reaction to the column on the right. Immediate hypersensitivity is mediated by IgE antibodies, which result in an allergy, anaphylaxis, or atopic disease. The NP should expect the client to have a type 1 hypersensitivity to recent medication use, which can include these immediate reactions as clinical manifestations: urticaria, wheezing, vomiting, and diaphoresis. Hypertension and bradycardia are not associated with immediate hypersensitivity reactions. Initiating a Hypersensitivity Reaction Complete the following sentence by choosing from the list of options. Mast cellsT-cells are the primary effector cells and responsible for initiating and mediating type 1 hypersensitivity reactions. Characterized by the rapid release of proinflammatory mediators like histamine, leukotrienes, and cytokines in response to allergen exposure, mast cells are the primary effector cells responsible for initiating and mediating type 1 hypersensitivity reactions. Pathology of a Hypersensitivity Reaction Complete the following sentence by choosing from the lists of options. Type 3 hypersensitivity reactions involve the formation of immune complexes that can deposit in tissues, leading to complement activation, inflammation, and tissue destruction. Type 3 hypersensitivity reactions involve the formation of immune complexes that can deposit in tissues, leading to complement activation and inflammation. This process can cause tissue damage and is associated with systemic lupus erythematosus (SLE) and serum sickness. Type 1 reactions are mediated by IgE antibodies, and type 2 are mediated by IgG or IgM antibodies. Type 4 reactions are activated by T-helper cells. Pathophysiology of Hypersensitivity Reactions There are four types of hypersensitivity reactions. The pathophysiology of each reaction depends on the underlying cause. Click each section below for an introduction to the four types of hypersensitivity reactions. Type 1 Hypersensitivity Reaction A type 1 reaction is mediated by IgE antibodies.  Anaphylactic Reaction 1. Antigen 2. B-cell 3. Plasma cell 4. IgE 5. Mast cell Histamine Type 2 Hypersensitivity Reaction A type 2 cytotoxic reaction is mediated by IgG or IgM antibodies. 1. Anti-A antibodies in type B blood mix with type A blood 2. Antibodies attach to surface antigen of type A RBC 3. Complement activated, type A RBC cell wall attacked 4. Lysis of type A RBC 5. Phagocytosis Type 3 Hypersensitivity Reaction A type 3 reaction is mediated by immune complexes.  Immune complex 1. Antibodies bind to antigens 2. Immune complexes form 3. Complexes deposit in blood vessels or tissues 4. Activation of complement 5. Inflammatory response at site of deposit 6. Release of lysosomal enzymes and chemical mediators 7. Tissue damage Type 4 Hypersensitivity Reaction A type 4 delayed reaction is mediated by cellular response. 1. Macrophage presents antigen 2. Sensitization of T lymphocyte 3. Release of lymphokines 4. Inflammation and lysis of antigen-bearing cells in the tissue  5. Tissue destruction Think Acid A: Allergic/Anaphylactic/Atopic (Type 1) C: Cytotoxic (Type 2) I: Immune Complex (Type 3) D: Delayed (Type 4) Pathophysiology of Type 1 Allergic Reaction Types of Hypersensitivity Reactions Localized Effect: When the immune system is first exposed to the antigen, it responds by forming IgE, which sensitizes the basophils and mast cells in tissues. During the second exposure to the same antigen, the immune system releases mediators (histamine). Vasodilation and increased permeability of blood vessels leads to inflammation, including edema, redness, and pruritus. Systemic Effect: When subsequent exposure to the same antigen occurs, the antigen binds with IgE antibodies. Mast cells release large amounts of histamine into general circulation. Cardiovascular system: Vasodilation and increased capillary permeability cause decreased blood pressure, faintness, or weakness. Skin nerve endings are irritated, leading to itching. In the lungs, constriction of bronchioles and release of mucus leads to airways obstruction, cough, or dyspnea. All these can cause severe oxygen deficit to the brain. Type 1 hypersensitivity reactions, also known as immediate hypersensitivity reactions, are characterized by the rapid release of proinflammatory mediators like histamine, leukotrienes, prostaglandins, and cytokines in response to allergen exposure. These local or systemic effects are mediated by IgE antibodies, which result in an allergic reaction, anaphylaxis, or atopic disease. Physiological manifestations include the following: vasodilation bronchial smooth muscle contraction mucus production The most common allergic reactions are type 1 reactions to environmental antigens (e.g., pollen, insects [bee venom], tree nuts, and medications). Allergic reactions can also occur to foods, latex, animal hair, and pet dander. Type 1: Allergic Rhinitis Allergic rhinitis, often referred to as hay fever, is a common type 1 hypersensitivity reaction and involves immunoglobulin E (IgE) mediated release of antibodies to the antigen. This results in mast cell degranulation, release of histamine, and other inflammatory mediators. Mast cells are the primary effector for initiating and mediating type 1 reactions. Examine the image to learn more about common symptoms and triggers of allergic rhinitis.  Symptoms and Triggers of Allergic Rhinitis (AR) Symptoms Itchy eyes or nose Sneezing Running nose Watering of the eyes Nasal congestion Allergic triggers Indoor ○ Dust mites ○ Animal dander ○ Cigarette smoke Outdoor ○ Mold spores ○ Pollen Clinical Application: Allergic Asthma J. S. is a 64-year-old female who presents to the primary care office with complaints of low back pain and burning on urination. She also indicates that she has been urinating frequently and has had to wear a pad because she also is experiencing urgency and she is afraid that she might “leak.” She tells the Nurse Practitioner (NP) that she suspects that she has a urinary tract infection (UTI). She reported that it has been at least 2 years since she had a UTI and was treated with an antibiotic but cannot remember its name. She denies any medication or food allergies. After conducting a thorough health history and physical exam, the NP diagnoses the patient with uncomplicated UTI and orders a course of sulfamethoxazole/trimethoprim (Bactrim DS). The next day, J. S. returns to the office in a panic to report she has just taken her first dose of the medication about an hour ago. She began to feel anxious followed by wheezing in the chest and dizziness. She first called her daughter, who reminded her that she is allergic to sulfa drugs. J. S. is immediately examined by the NP. The subjective and objective findings are: Subjective: Anxious Dizziness Wheezing Objective: Vital signs: BP 90/50, HR 112 Red rash on chest and anterior neck Swelling around the right eye Wheezing with airflow throughout lung fields When analyzing clients symptoms, the nurse practitioner (NP) relies on pathophysiology to explain the cause of the symptoms. Once the underlying reasons for the symptoms are identified, the NP can make an accurate diagnosis and select appropriate treatment. Note that our client is experiencing both localized symptoms (rash on chest and anterior neck and right eye swelling) and systemic symptoms (wheezing and hypotension). Let’s use our knowledge of pathophysiology to explain why she is having these presenting symptoms. The NP quickly identifies this as an allergic reaction and immediately asks the client again if she is aware of any prior allergies to medications. The client tells the NP that her daughter reminded her that she is allergic to sulfa drugs. The sulfamethoxazole, in this case, is considered the allergen to which the client has become sensitized from the last time she was treated for a UTI. At the time that she became sensitized, the IgE antibodies attached to the cells that became sensitized; then at the time of further exposure, IgE caused the sensitized cells to degranulate. When degranulation occurs, inflammatory mediators like histamine, leukotrienes, and prostaglandins are released to produce several effects on the body. Vasodilation occurs which explains the client’s hypotension, dizziness, and rash. At this point, inflammatory mediators are released. These include histamine, leukotrienes, and prostaglandins. Constriction of bronchial smooth muscle also occurs, which explains her respiratory symptom of wheezing. Based on the localized and systemic symptoms, the NP can diagnose the client with anaphylactic reaction, a Type I hypersensitivity reaction. Allergic Rhinitis: Recognizing Risk Factors Highlight the finding(s) the nurse practitioner (NP) recognizes as risk factors that may contribute to the client’s new diagnosis of allergic rhinitis. Select all that apply. Camille Rutherford, 45-years-old Chief Complaint: red, dry, itchy skin on arms and legs, shortness of breath, wheezing, and cough Medical History: presents with a nonproductive cough, expiratory wheezing, and shortness of breath upon exertion; reports a gradual onset of these symptoms and mentioned that they have been progressively worsening when walking their dog outside Past Medical History: eczema, hypertension Social History: lives at home with daughter and their dog Allergic rhinitis attacks are related to ongoing exposure to specific offending agents. The strongest risk factor for developing asthma is a history of atopic disease (the client has eczema, a form of atopic dermatitis). Environmental factors and allergens—such as high humidity, cold, dry weather, house dust mites, pet fur, and pollen—can place a client at risk for a new diagnosis of allergic asthma. With prior exposure to allergens, Camille was sensitized. Chronic exposure to allergens mediated IgE antibodies to attach to sensitized cells, and with further exposure, IgE caused sensitized cells to degranulate. When degranulation occurs, inflammatory mediators like histamine, leukotrienes, and prostaglandins are released to produce several effects on the body, such as shortness of breath and wheezing. Constriction of bronchial smooth muscle also occurs, which explains her respiratory symptoms: shortness of breath, cough, and wheezing. The NP can diagnose the client with a type I hypersensitivity reaction based on localized and systemic symptoms. The client’s age and history of hypertension are not risk factors. Pathophysiology of Type 2 Hypersensitivity Reaction Type 2 hypersensitivity reactions are immune reactions against a specific cell or tissue. Cells express various antigens on their surfaces, while others are expressed on the membranes of only specific cells (called tissue-specific antigens). Altered tissue-specific antigens are bound by autoantibodies, resulting in tissue destruction by macrophages, neutrophils, natural killers, or complement cells. The symptoms of many type 2 reactions are determined by the tissue or organ that expresses the antigen. For example, heparin-induced thrombocytopenia (HIT) is a tissue reaction where the immune system causes your platelets to clot when introduced to heparin, which puts a client at risk of developing life-threatening blood clots. It also results in platelet levels dropping (thrombocytopenia) and the risk of uncontrolled bleeding. Cytotoxic hypersensitivities can occur with hemolytic transfusions. The client’s blood must be typed and cross-matched to prevent possible cytotoxic hypersensitivities. Type 2 Cytotoxic Hypersensitivity 1. Anti-A antibodies in type B blood mix with type A blood. 2. Antibodies attach to the surface of antigen of type A blood. 3. Complement is activated, and type A blood cell wall is attacked. 4. Lysis of type A blood occurs. 5. Phagocytosis occurs when the macrophage consumes the destroyed type A blood. Type 2: Graves' Disease Graves’ disease symptoms include bulging eyes, enlarged thyroid (goiter), arrythmia and tachycardia, nausea and diarrhea, tremor, change in menstrual cycles (in females), muscle weakness, headache, weight loss, anxiety and irritability, and increased perspiration. Macrophages are the primary effector cells of type 2 responses. A type 2 hypersensitivity response begins with the antibody binding to the antigen and may cause the following: the cell to be destroyed by the antibody cell destruction through phagocytosis by macrophages damage to the cell by neutrophils triggering phagocytosis natural killer cells to release toxic substances that destroy the target cell malfunction of the cell without destruction For example, Graves' disease is caused by the production of IgG autoantibodies that bind to and stimulate the thyroid-stimulating hormone (TSH) receptor on thyroid follicular cells. This causes cellular malfunction without destruction, thyroid gland growth, and an overproduction of thyroid hormones (hyperthyroidism). Clinical Application: Type 2 - Hemolytic Transfusion Reaction A hemolytic transfusion reaction is a severe complication that can occur after a blood transfusion. The transfused red blood cells (RBCs) are destroyed by the client’s immune system. M. G., a 27-year-old healthy female, required a blood transfusion 4 hours post-partum after undergoing a C-section. Twenty-four hours later, she and her newborn were released from the hospital in good health. Approximately 1 week later, she came to the primary care office complaining of fever, chills, shortness of breath (dyspnea), and a backache. The nurse practitioner (NP) conducts an exam and the subjective and objective findings reveal the following: Subjective: Fever Chills Shortness of breath (dyspnea) Backache Objective: Fever 100.1 °F (37.8 °C) Blood pressure 100/64 mmHg Pulse 110 bmp Respirations 20/min Scleral icterus Lab Work:  Hemoglobin 6.2 Platelet and leukocyte count are normal Positive direct and indirect Coombs test—revealed the presence of antibodies Once again, let’s rely on our knowledge of pathophysiology to explain why M. G. is presenting with these symptoms. The NP notes that the only new occurrence with the client was the blood transfusion that she received approximately a week ago post-partum. In delving deeper into the client’s history, the NP learned that M. G. had a blood transfusion during her first C-section two years ago. This provides a great clue for the NP to consider the cause of M. G.’s current symptoms. At the time of the first transfusion, M. G.’s RBCs became sensitized. Upon the second transfusion two years later, IgG recognized the sensitized cells and initiated an immune response. In essence, IgG recognized the sensitized cells as non-self-antigens. The destruction of the RBCs resulted in her jaundice (scleral icterus), low hemoglobin level, and fever. Treatment for a delayed hemolytic reaction will most likely require a blood transfusion that does not contain the antigen. Eventually, the mismatched blood is replaced with blood that is compatible with M. G.’s blood. Pathophysiology of Graves’ Disease A 25-year-old presents to the emergency department (ED) with symptoms of ongoing weight loss, rapid heart rate, bilateral neck swelling, and hand tremors. Family medical history reveals a history of thyroid disorders. Physical examination and laboratory tests confirm the diagnosis of Graves' disease. Which mechanism below best explains the pathophysiology of Graves’ disease? Delayed-type hypersensitivity response in the thyroid gland Production of autoantibodies targeting the thyroid-stimulating hormone receptor Activation of complement proteins leading to tissue damage Formation of immune complexes in the thyroid tissue Graves’ disease is an example of a type 2 hypersensitivity reaction in which the immune system produces autoantibodies, particularly IgG antibodies, that bind to and stimulate the thyroid- stimulating hormone (TSH) receptor on thyroid follicular cells. This leads to excessive thyroid hormone production, hyperthyroidism, and the characteristic symptoms observed in the client. Cytotoxic antibodies target specific cell surface antigens (in this case, the TSH receptor), resulting in cellular dysfunction rather than cell destruction. Pathophysiology of Type 3 Immune-Complex Mediated Reactions For clients with type 3 immune-complex mediated reactions, antibodies are formed to antigens circulating in the blood, resulting in immune complexes that deposit in tissues. These immune complexes activate complement and neutrophil cells, resulting in tissue destruction. The major difference between type 2 and type 3 responses is that in a type 2 response, the antibody binds to the antigen on the cell surface, but in type 3 responses, the antibody binds to the antigen in the blood or body fluids and then circulates to the tissue. Type 3 reactions are not organ-specific and use neutrophils as the primary effector cell. In Type 3 hypersensitivity reactions, immune-complex deposition (ICD) causes autoimmune diseases, which is often a complication. As the disease progresses, immune complexes accumulate, deposit, and overload the tissue. As the phagocytes, erythrocytes, and complement systems fail to remove excess immune complexes, inflammation sets in. Common immune system-complex reactions include systemic lupus erythematosus (SLE), serum sickness, and what is known as the Raynaud phenomenon (a form of serum sickness). Type 3 Immune Complex Hypersensitivity 1. Antibodies bind to antigens 2. Immune complexes form 3. Complexes deposit in blood vessels or tissues 4. Activation of complement 5. Inflammatory response at the site of deposit 6. Release of lysosomal enzymes and chemical mediators 7. Tissue damage Type 3: Systemic Lupus Erythematosus  Mouth sores Muscle and joint pain Fever Memory issues Hair loss Rashes Kidney problems High blood pressure Anemia and blood clotting Fatigue Light sensitivity Systemic lupus erythematosus (SLE) is an autoimmune, type 3 hypersensitivity reaction in which the body’s immune system attacks its own tissues and organs. In SLE, B- and T-cells become overactive, increasing the production of autoantibodies and activating the complement system and neutrophils. This results in widespread inflammation, tissue destruction, and scar formation and can affect many body systems. Clinical manifestations may be mild, develop slowly, come on suddenly, and be severe enough to require hospitalization. Clinical Application: Type 3 Immune-Complex Reaction – Serum Sickness Serum sickness is an immune-complex hypersensitivity reaction that presents with fever, rash, generalized joint pain, and localized swelling. A young mother brings her 5-year-old daughter to the primary care clinic with a fever of 102 °F (38.89 °C) degrees, swollen hands and knees, “achy” joints, and a red rash on her legs. The NP remembers that she recently diagnosed the patient with strep throat and started her on amoxicillin for 10 days. The mom confirms that she started the amoxicillin on the same day that her daughter was diagnosed and has been taking it for the last 7 days. Mom indicated that she stopped giving the client the antibiotic yesterday for fear that she may be having a drug reaction. However, the presenting symptoms continued. Client’s temperature in the office is 102 °F (38.89 °C). The NP diagnoses the client with serum sickness. The NP conducts an exam and the subjective and objective findings reveal the following: Subjective: Fever Rash Generalized joint pain Swollen hands and feet Objective: Fever Non-blanching red rash Swollen fingers bilaterally Swollen knees bilaterally This client presents with the classic symptoms of serum sickness. Immune complexes are formed in response to an antigen (amoxicillin) that has been taken into the body. These complexes deposit themselves into the vascular endothelium causing vasculitis and tissue injury as a result of complement. The skin and joints are most commonly affected. Fortunately, the condition is self-limiting. Type 3 Reaction Sequence in Order Drag and drop the pathophysiological processes of a type 3 immune complex hypersensitivity into the correct order. Antibodies bind to antigens Immune complexes form Complexes deposit in blood vessels or tissues Activation of complement Inflammatory response at the site of deposit  Release of lysosomal enzymes and chemical mediators Tissue damage The pathophysiological processes of a type 3 immune complex hypersensitivity in the correct order are as follows: 1. Antibodies bind to antigens 2. Immune complexes form 3. Complexes deposit in blood vessels or tissues 4. Activation of complement 5. Inflammatory response at the site of deposit 6. Release of lysosomal enzymes and chemical mediators 7. Tissue damage Pathophysiology of Type 4 Cell-Mediated, Delayed Reaction Type 4 hypersensitivity reactions are delayed, cell-mediated responses mediated by T- lymphocytes and macrophages. When the individual encounters the antigen, T-cells are activated and move to the area of the antigen. The antigen is taken up, processed, and presented to macrophages, leading to epidermal reactions characterized by erythema, cellular infiltration, and vesicles. T-cells and macrophages sometimes cannot destroy or remove an offending antigen, leading them to encase and contain the invader by forming a granuloma. The formation of multiple granulomas can lead to tissue damage and organ dysfunction. A type 4 reaction can also be present in other autoimmune diseases. For example, T-cell response to type 2 collagen can lead to joint damage in clients with rheumatoid arthritis (RA). T- cell response to an antigen on the surface of pancreatic beta cells contributes to beta-cell destruction in clients with insulin-dependent (type I) diabetes mellitus.  Type 4 Cell-Mediated or Delayed Hypersensitivity 1. Macrophage presents antigen 2. Sensitization of T lymphocyte 3. Release of lymphokines 4. Inflammation and lysis of antigen-bearing cells in the tissue 5. Tissue destruction Clinical Application: Contact Dermatitis Contact dermatitis is an eczematous, cutaneous skin condition exacerbated by exposure to various foods and environmental allergens. Clients report dryness with pruritus, in which scratching can create or exacerbate open lesions, putting them at risk for infection. J. S. is a 17-year-old male who plays high school football. Last weekend, the team played an out of town game. On the way home from the game, the team bus was stopped because of a fallen tree and other types of brush blocking the road after a severe thunderstorm. J. S. and his teammates removed debris from the road and then proceeded on their trip home. Three days later, while sitting in his math class, he develops severe itching and a rash over his hands, arms, and neck. Later that day, his mother takes him to see the nurse practitioner (NP) at the primary care office. She asks him to share any unusual exposures that he has recently encountered, and he informs her about contact with the road debris a few days earlier. The NP conducts an exam and the subjective and objective findings reveal the following: Subjective: Itchy rash Objective: Thickened patches with some crusting and oozing of clear fluid Contact dermatitis is a classic type 4 hypersensitivity reaction that occurs after an exposure to the skin. The symptoms typically appear a few days later. This is a T-cell-mediated response that is initiated when the individual comes into subsequent contact with the antigen. It is possible that he has been exposed prior to the appearance of the rash. On the current exposure, the T-cell recognizes the antigen and causes the classic immune reaction. The macrophages begin phagocytosis, which leads to the skin reaction of erythema and the formation of vesicles. To reduce the itching and rash, a high potency steroid topical cream can be prescribed. Sometimes systemic steroids may be indicated if a large area of the face or other body surfaces are involved. Poison Ivy Exposure A client presented to the primary care office with a generalized rash and epidermal blistering from contact exposure to poison ivy two days ago. The nurse practitioner (NP) suspects a hypersensitivity reaction. What clinical manifestations should the NP consider to differentiate a type 1 hypersensitivity rash from a type 4 hypersensitivity rash? A type 1 hypersensitivity rash is often localized and erythematous, whereas the rash in type 4 hypersensitivity is generalized and pruritic. A type 1 hypersensitivity rash often involves hives or urticaria, while a delayed onset, epidermal blistering rash characterizes a type 4 reaction. A type 1 hypersensitivity rash is usually associated with contact dermatitis, while the rash in a type 4 hypersensitivity reaction is commonly seen in allergic reactions. A type 1 hypersensitivity rash results from T-cell-mediated inflammation, whereas the rash in a type 4 hypersensitivity reaction is primarily due to the activation of mast cells. Type 4 hypersensitivity reactions are T cell-mediated delayed hypersensitivity reactions, have a delayed onset, and the rash is often characterized by epidermal blistering. T-cells are central in recruiting other immune cells and causing inflammation in response to an antigen. Type 1 hypersensitivity reactions typically involve activating mast cells and basophils, releasing histamine and other inflammatory mediators. This can result in localized erythema (redness) and the formation of hives or urticaria. Life-Threatening Allergic Reactions Anaphylaxis is a systematic, life-threatening allergic reaction that is potentially fatal, characterized by airway obstruction and hypotension. A client who is highly sensitive to the antigen may experience anaphylaxis. Most common anaphylactic reactions are due to food ingestion (eggs, shellfish, peanuts, drug reactions) and insect venom. Anaphylaxis: Facial Swelling Anaphylaxis is a severe, systemic allergic reaction characterized by swelling of the face, tongue, throat, or airways. Swelling and constriction of the throat and airways can lead to wheezing and difficulty breathing. Other symptoms of anaphylaxis include hives, flushed skin, nausea, and dizziness. Anaphylaxis is caused by the body's immune response to an allergen. Allergens are harmless substances that cause an overactive response in some individuals. Common allergens include foods such as nuts or shellfish, certain medications, insect stings, and latex. When a person with an allergy comes in contact with their allergen trigger, white blood cells such as mast cells release chemicals to attack the allergen. One of the chemicals released during anaphylaxis is histamine. Histamine causes the dilation (widening) of blood vessels and increases heart rate and gland secretion. Other chemicals released during the immune response cause constriction of the airways and increase the permeability of blood vessels. Together, these chemicals cause the suite of symptoms associated with anaphylaxis. Anaphylactic Treatment Review the algorithm for anaphylaxis treatment. Treating an anaphylactic reaction is a medical emergency as the airway can be compromised quickly.  Algorithm for Anaphylaxis Treatment Manage exposure Remove the client from a known or suspected allergen. Assess airway, breathing, and circulation Confirm anaphylaxis One of the following three criteria is met within minutes to 2–3 hours following possible allergen exposure Criteria 1: Acute onset of an illness with involvement of the skin-mucosal tissues (hives, pruritis or flushing, swelling of face, lips, tongue) and at least one of the following ○ Respiratory distress ○ Reduced blood pressure or associated symptoms of end-organ dysfunction ○ Significant gastrointestinal symptoms (abdominal pain and/or vomiting) Criteria 2: two or more of the following that occur rapidly after exposure to a likely allergen: ○ Involvement of the skin mucosal tissue ○ Respiratory distress ○ Reduced blood pressure or associated symptoms of end-organ dysfunction ○ Significant gastrointestinal systems (abdominal pain and/or vomiting) Criteria 3: reduced blood pressure after exposure to a known allergen  ○ Initial Intervention ○ If the criteria for anaphylaxis are met, administer epinephrine intra-muscularly in the anterolateral thigh immediately. EpiPen Auto-Injector dose is 0.3 mg for adults and children greater than 25 kg; EpiPen Jr Auto-Injector is 0.15 mg for children 5-25 kg ○ Repeat epinephrine dose every 5-15 minutes as needed if the following symptoms continue: Signs of upper airway obstruction Continued respiratory distress Poor perfusion or hypotension Significant gastrointestinal symptoms Place in supine position with lower extremities elevated Initiate emergency response per protocol Monitoring and additional interventions Monitor vital sign continuously Consider supplemental oxygen and normal saline intravenous fluid Cardiopulmonary resuscitation should be performed if indicated Event documentation Document the known allergen and response while waiting for emergency responders Type of Allergic Reaction For each hypersensitivity reaction, click to specify which immunologic mechanism (type 1, 2, 3, 4) causes the clinical condition. Type Name Mechanism of Hypersensitivity Clinical Examples 1 Immunoglobulin E (IgE)- T helper 2 cells produce high levels Allergic rhinitis, Asthma, mediated reaction of interleukin-4, leading to B-cell Anaphylaxis activation and subsequent plasma cell production of IgE antibody. IgE binds to mast cell receptors resulting in their immediate degranulation and release of histamine, leukotrienes, and other inflammatory mediators. 2 Tissue-specific reaction Altered self-antigens on tissues are Autoimmune hemolytic bound by autoantibodies resulting anemia, Heparin-induced in tissue destruction by thrombocytopenia, Graves' complement, macrophages, disease, Myasthenia gravis neutrophils, or natural killer cells. Some autoantibodies bind to hormone or neurotransmitter receptors causing decreased or increased receptor activation. 3 Immune complex- Antibodies are formed to circulating Systemic lupus mediated reaction antigens resulting in the formation erythematosus, Raynaud of immune complexes that deposit phenomenon in tissues. These immune complexes activate complement and neutrophils resulting in tissue destruction.  4 Cell-mediated reaction T helper 1 cells produce interferon Contact sensitivity to poison gamma resulting in the activation of ivy and latex, Mycobacterial macrophages and T cytotoxic cells infection that attack the target cell through the release of destructive enzymes. In some cases, destruction of an invader is not possible, and granuloma formation walls it off from the rest of the body. Case Study: Hypersensitivity The following six questions are part of an unfolding case study. History and Physical Chief Complaint: Joint pain, rash, and fatigue Allergies: Non-steroidal anti-inflammatory drugs (NSAIDs) (difficulty breathing) History of Present Illness: 28-year-old female, admitted to the telemetry unit for exacerbation of systemic lupus erythematosus (SLE). Reports 102 °F (38.8 °C) fever for last 2 days Review of Systems: General: Fatigue Neurological: Alert and oriented to person, place, time, and situation (A&O x 4); Pupils equal, round, reactive to light, and accommodation (PERRLA) Cardiovascular: Sinus tachycardia on cardiac monitor; Regular rate. S1 and S2 present Respiratory: Respirations even and unlabored at rest; Lungs clear to auscultation (CTA) Gastrointestinal: Reports regular, daily bowel movements. Denies abdominal pain Genitourinary: Denies urinary symptoms. Last menstrual period (LMP) 2 weeks ago Integumentary: Skin pink, warm, and dry. Rash covering cheeks and bridge of the nose; dry red patches with purulent drainage on the face; no bruising noted Musculoskeletal: Reports muscle weakness and joint pain 5/10 on pain scale Home Medications: Phenytoin, birth control, ferrous sulfate, acetaminophen as needed (PRN) PROGRESS NOTES 0900 Assisting client to the restroom. Upon standing, the client became dizzy and needed to sit back down on the bed. Blood pressure taken after client sat back down was 100/58 mmHg and heart rate was in the 120s on the cardiac monitor when client stood up. Client reported feeling slight palpitations. Notified nurse practitioner. Labs Standard Values Results White Blood Cells (WBCs) 4,000-10,000 mm³ 2,250 mm³ Red Blood Cells (RBCs) 4.2-5.9 cells/L 4.2-5.9 cells/L Hemoglobin (Hgb) 12.0-17.0 g/dL 10.1 g/dL Hematocrit (Hct) 36-51% 30% Platelets 150,000-350,000 mm³ 175,000 mm³ Sodium 135-145 mEq/L 142 mEq/L Potassium 3.5-5.0 mEq/L 4.5 mEq/L Calcium 9-10.5 mg/dL 9.8 mg/dL Chloride 98-106 mEq/L 98 mEq/L Blood urea nitrogen (BUN) 8-20 mg/dL 15 mg/dL Creatinine 0.7-1.3 mg/dL 1.1 mg/dL Glucose 70-100 mg/dL 88 mg/dL Erythrocyte sedimentation rate (ESR) 0-20 mm/hr 35 mm/hr C-reactive protein (CRP)