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Jun 13, 2024

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EDAPT- Hypersensitivity Reactions 1. Hypersensitivity Reactions a. The immune system functions to eliminate pathogens from the body using various mechanisms. A pathogen is just simply a bacterium, virus or other microorganism that can cause disease. These mechanisms typically create a localized inflammatory response that effectively eliminates the pathogen without minimal damage to the surrounding tissue. Besides pathogens, individuals come into contact with numerous foreign antigens, such as plant pollen and food. Contact with these environmental antigens does not elicit an immune response in the majority of individuals. However, in certain predisposed individuals, the immune system can mount a response to these generally innocuous antigens, resulting in tissue damage that ranges from mild irritation to life- threatening anaphylactic shock. These immune responses are referred to as allergic reactions or hypersensitivity reactions. Hypersensitivity reactions can be divided into four categories, Type I to Type IV, distinguished by the cell types and effector molecules involved. 2. Contact Dermatitis is an example of Type 4 hypersensitivity reaction. a. Allergic contact dermatitis is an example of a Type IV hypersensitivity reaction mediated by T-cells. When the individual comes in contact with the antigen (e.g. poison ivy), an antigen complex is formed. On subsequent exposure to the antigen, sensitized T-cells activate the inflammatory process that causes the allergic contact dermatitis to appear. 3. Anaphylaxis is a Type 1 hypersensitivity reaction. a. Type 1 hypersensitivity reactions are mediated by IgE and mast cells. An individual who is highly sensitized to the antigen may experience anaphylaxis. 4. Type 2 (cytotoxic) hypersensitivity reactions are mediated by: IgG or IgM . a. The Type 2 hypersensitivity reaction is mediated by IgG or IgM. 5. Which of the following are considered the “first responders” of the innate immune system? Neutrophils a. Neutrophils appear first in any immune response. 6. Hives (urticaria) ar an example of a: Type 1 hypersensitivity reaction a. Hives (urticarial) are an example of a Type 1 hypersensitivity reaction mediated by the antibody, IgE and mast cells. 7. Type 1: Allergic Reaction a. On initial encounter with an allergen, the individual will first produce IgE antibodies. After the allergen is cleared, the remaining IgE molecules will be bound by mast cells, basophils, and eosinophils that contain receptors for the IgE molecules. This process is referred to as sensitization. On subsequent exposure to the allergen, the IgE molecules located on the sensitized cells induces their immediate degranulation. This causes the release of inflammatory mediators such as histamine, leukotrienes, and prostaglandins that results in vasodilation, bronchial smooth muscle contraction, and mucus production. Type I hypersensitivity reactions can be local or systemic. Systemic reactions can result in anaphylaxis, a potentially life-threatening condition. Allergic asthma is an example of a Type I hypersensitivity reaction. On exposure to certain allergens (typically inhaled), individuals with allergic asthma experience inflammation of the airways,

characterized by tissue swelling and excessive mucus production. This narrowing of the airways makes it difficult to breathe. i. Example of Allergic Asthma: 1. 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). 2. 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. 3. The NP performs a thorough exam and finds the following: a. Subjective Findings : Anxious, Dizziness, Wheezing b. Objective Findings : red rash on chest and anterior neck, swelling around the right eye, wheezing with airflow throughout lung fields, bp 90/50, hr 112 4. When analyzing patient 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. 5. Note that our patient is experiencing both localized symptoms (rash on chest and anterior neck and right eye swelling) and systemic symptoms (wheezing and hypotension). 6. The NP quickly identifies this as an allergic reaction and immediately asks the patient again, if she is aware of any prior allergies to medications. The patient tells the NP that her daughter reminded her that she is allergic to sulfa drugs. The Bactrim, in this case, is considered the allergen to which the patient has become sensitized from the last time she was treated for a UTI. 7. At the time that she became sensitized, the IgE antibodies attached to the cells that became sensitized and 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 patient’s hypotension, dizziness and rash).

8. 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 patient with anaphylactic reaction, a Type 1 hypersensitivity reaction. 8. Type 2 Hypersensitivity Reaction a. Type II hypersensitivity reaction is tissue-specific and usually occurs as a result of haptens that cause an IgG antibody or IgM antibody mediated response. The antibodies are specifically directed to the antigen located on the cell membrane. A hapten is a small molecule that can cause an immune response when it attaches to a protein. Macrophages are the primary effector cells of Type II responses. Typical examples of Type II reactions are drug allergies, as well as allergies against infectious agents. The Type II response begins with the antibody binding to the antigen and may cause the following. i. The cell to be destroyed by the antibody ii. Cell destruction through phagocytosis by macrophages iii. Damage to the cell by neutrophils triggering phagocytosis iv. Natural killer cells to release toxic substances that destroy the target cell v. Malfunction of the cell without destruction b. Examples of type II reactions include drug allergies, hemolytic anemia, blood transfusion mismatch with resulting transfusion reaction and Rh hemolytic disease. i. Ex: Clinical Application of Delayed Hemolytic transfusion reaction 1. 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. 2. The NP conducts an exam and the subjective and objective findings reveal the following: a. Subjective : fever, chills, shortness of breath, backache b. Objective : Fever 100.1, bp 100/64, pulse 110bpm, rr20/min, scleral icterus c. Lab work : hemoglobin 6.2, platelet and leukocyte count are normal, positive direct and indirect Coombs Test (revealed the presence of antibodies). 3. Once again, let’s rely on our knowledge of pathophysiology to explain why she is presenting with these symptoms. The NP notes that the only new occurrence with the patient was the blood transfusion that she received approximately a week ago post-partum. In delving deeper into the patient’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.

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4. At the time of the first transfusion, M.G.’s RBC’s 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. 9. Type 3 Immune-Complex Reaction a. The Type III hypersensitivity reaction is also an antigen-antibody response. The major difference between Type II and Type III responses is that in a Type II response, the antibody binds to the antigen on the cell surface, but in Type III responses, the antibody binds to the antigen in the blood or body fluids and then circulates to the tissue. Type III reactions are not organ specific and use neutrophils as the primary effector cell. In type III hypersensitivity reactions immune-complex deposition (ICD) causes autoimmune diseases, which is often a complication. As the disease progresses a more accumulation of immune-complexes occurs, and when the body becomes overloaded the complexes are deposited in the tissues and cause inflammation as the mononuclear phagocytes, erythrocytes, and complement system fail to remove immune complexes from the blood. One of the classic Type III reactions is serum sickness. i. Ex: Clinical Application of Serum Sickness 1. A young mother brings her 5-year old daughter to the primary care clinic with a fever of 102 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 patient the antibiotic yesterday for fear that she may be having a drug reaction. However, the presenting symptoms continue. Patient’s temperature in the office is 102 degrees. The NP diagnoses the patient with serum sickness. 2. The NP conducts an exam and the subjective and objective findings reveal the following: a. Subjective : fever, rash, generalized joint pain, swollen hands and feet. b. Objective : fever, non-blanching red rash, swollen fingers bilaterally, swollen knees bilaterally. 3. This patient 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. 10. Type 4 Cell-Mediated, Delayed Reaction a. The type IV hypersensitivity reactions are known as cell-mediated responses and use lymphocytes and macrophages as primary mediators. Unlike the first three types of responses, which are humoral immune functions, a Type IV response is mediated by T- lymphocytes and does not use antibodies. A typical reaction from a Type IV cell- mediated response would be a localized contact dermatitis. When the individual comes in contact with 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. i. Ex: Clinical application of contact dermatitis 1. 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. 2. 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 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. 3. The NP conducts an exam and the subjective and objective findings reveal the following: a. Subjective : itchy rash b. Objective : Thickened patches with some crusting and oozing of clear liquid. 4. Contact dermatitis is a classic type IV 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. 11. Summary of Hypersensitivity Reactions a. In summary, we reviewed the four types of hypersensitivity reactions. For each type, the pathophysiology was reviewed. Clinical applications were provided that illustrated the need to understand the underlying pathophysiology in order to explain the symptoms and select appropriate treatment.

Type Mechanism Example Pathology 2 Tissue-specific destruction or impairment because of:  Antibody binding followed by lysis via complement  Antibody binding followed by macrophage phagocytosis  Antibody binding followed by neutrophil destruction  Antibody-dependent cell (NK)- mediated cytotoxicity, or  Antireceptor antibodies 1- ABO Incompatibility 5- Graves’ Disease 1- Complement damages RBC membrane and cells lyse 5- Autoantibodies specific for thyroid tissue impair receptor for TSH. 4 Cytotoxic T Cell-Mediated Contact Dermatitis (ex: poison ivy) T cells attack tissue directly (no antibody) 1 IgE action on mast cells Hay Fever (Allergic Rhinitis) Mast cell degranulation results in an inflammatory response 3 Antigen-Antibody complex deposited in tissues Raynaud’s phenomenon Complex deposited in small peripheral vessels in cool temperatures leading to vasoconstriction and blocked circulation 12. Bee Stings a. The diagnosis for an individual who presents to the office with sudden swollen lips and eyes, shortness of breath and throat tightness after a bee sting is: Anaphylaxis i. The symptoms are consistent with the life-threating condition, anaphylaxis after being exposed. to a bee sting. 13. Type 4 Mediations a. Type 4 cytotoxic hypersensitivity reactions are mediated by: T-cells i. The Type IV hypersensitivity reaction is mediated by T-cells. 14. ABO Incompatibility a. Damage occurs with ABO incompatibility because: complement damages RBC membrane causing cell lysis i. The damage from ABO incompatibility occurs because of the effects of complement on the RBC membrane that results in RBC lysis. 15. Urticaria a. Which of the following assessment findings would be expected in a patient who presents with urticaria: Eosinophilia i. Eosinophils are present in the allergic reaction EDAPT- Immunodeficiency 1. Primary Immunodeficiency a. An example of a primary immunodeficiency is: Chronic Granulomatous Disease

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i. Chronic granulomatous disease (CGD) is an example of a primary immunodeficiency. 2. Autoimmune Disease a. Which of the following is an autoimmune disease: Systemic Lupus Erythematosus (SLE) i. Systemic Lupus Erythematosus (SLE) is an example of an autoimmune disease. 3. Secondary Immunodeficiency a. An example of a secondary immunodeficiency is: Pneumocystis Carinii i. Pneumocystis Carinii is an example of a secondary immunodeficiency. It is caused by something external to the immune system; in this case, a yeast-like fungus. 4. Secondary immunodeficiency a. Malnutrition is a predominant cause of secondary immune deficiencies worldwide. i. Malnutrition is the predominant cause of secondary immune deficiencies worldwide. 5. Primary vs Secondary Immunodeficiences a. Immunodeficiencies are classified as either primary or secondary. Diseases Primary Secondary Chronic Granulomatous Disease of Childhood X DiGeorge Syndrome X Human Immunodeficiency Virus X Pneumocystis Carinii X Familial Mediterranean Fever X Pneumonia X Job Syndrome (Autosomal dominant hyper-IgE Syndrome) X Common Variable Immunodeficiency X Sinus Infection X Lung Cancer X b. Primary Immunodeficiency i. Primary immunodeficiencies are less common and occur due to a defect on the development of the immune system. This could involve antibody deficiencies, B- and T-cell deficiencies, defects in the phagocytic cells and deficiency of complement. c. Secondary Immunodeficiency i. Secondary immunodeficiencies are conditions where the immune system becomes compromised because of something else. It could be caused by cancer, an effect from a drug, such as chemotherapeutic agents that suppress the immune system and infections that compromise the immune system in a profound way. ii. A common secondary immunodeficiency in the U.S. is Human Immunodeficiency Virus (HIV). HIV is an RNA virus that invades the body through any cell in the

body by direct contact of an individual’s blood or body secretions. The virus has a strong affinity for cells of the immune system, especially the CD4+ T-cells. Once the virus invades, it replicates to cause extensive damage to the immune system. Without a normally functioning immune system, the individual becomes susceptible to opportunistic infections, cancer, neurological diseases, wasting and death. iii. Cancer is another type of secondary immunodeficiency.See the presentation on the Biology of Cancer that was downloaded and saved in week 1 file. 1. Benign characteristics : grow slowly, well-defined capsule, not invasive, well differentiated, low mitotic index (percentage of cells in active division), do not metastasize. 2. Malignant Characteristics : grow rapidly, not encapsulated, invasive, poorly differentiated, high mitotic index (percentage of cells in active division), can spread distantly (metastisis). a. Carcinoma (90%): epithelial cells of organ surfaces and linings b. Adenocarcinoma : ductal or glandular structures. c. Sarcoma (2%): connective tissue (bone/muscle) d. Leukemia or lymphoma (8%): blood and lymphatic systems e. Carcinoma in situ (CIS) : pre-invasive epithelial malignant tumor of glandular or epithelia origin that has not broken through the basement membrane or invaded the surrounding stroma. Can remain stable, progress to metastasis, or regress. f. Staging : microscopic analysis of biopsy tissue is done i. Stage 1: no evidence of metastasis ii. Stage 2: local invasion iii. Stage 3: spread to regional structures iv. Stage 4: distant metastasis v. Tumor staging using th tumor, nodes, metastasis (TNM) system is also done to help determine treatment options and prognosis. 1. T=primary tumor; the number equals size of tumor and its local extent. The number can vary according to site. a. T0=breast free of tumor b. T1= lesion <2cm in size c. T2= lesion 2-5cm d. T3= skin and/or chest wall involved by invasion. 2. N= lymph node involvement; a higher number means more nodes are involved. a. N0= no axillary nodes involved b. N1= mobile nodes involved c. N2= fixed nodes involved 3. M= extent of distant mestastasis

a. M0= no metastasis b. M1= demonstable metastasis c. M2= suspected metastasis 6. Formation of Cancer a. The formation of cancer begins with cell transformation and other factors. b. See video biology of cancer: cell transformation 7. Carcinogenesis and Metastasis a. See video biology of cancer: carcinogenesis and metastasis 8. Cancer prevalence and Risk a. See video cancer prevalence and risk 9. Primary Immunodefiency a. Select the best statement that best describes a primary immunodeficiency: Are less common and occur due to a defect on the development of the immune system . i. A primary immunodeficiency is due to a defect of the development of the immune system. 10. Cancer a. Cancer is a secondary immunodeficiency. True i. Cancer is a type of secondary immunodeficiency. 11. Human Immunodeficiency Virus a. A patient with human immunodeficiency virus (HIV) was admitted to the acute care facility with difficulty breathing. He is diagnosed with Pneumocytis carinii. Pneumocystis carinii an example of: Secondary immune disease i. Pneumocystis carinii is an example of a secondary immune disease due the having HIV. HIV has compromised the patient increasing susceptibility to invasion by opportunistic organisms 12. Chronic Granulomatous Disease a. A patient with Chronic Granulomatous Disease of Childhood has a primary immune disease i. Chronic Granulomatous Disease is a primary immunodeficiency that results from severe X-linked or autosomal defects in the respiratory system. EDAPT- Autoimmunity 1. Systemic Lupus Erythematosus a. The Antinuclear Antibody (ANA) test is positive in 90% of patients diagnosed with Systemic Lupus Erythematosus (SLE). i. 90% of patients diagnosed with SLE will have a positive ANA. b. Which of the following findings can be used to diagnose Systemic Lupus Erythematosus (SLE)? Facial rash confined to the cheeks i. A rash confined to the checks is common in SLE. 2. Normal Immune Function a. Which of the following can depress a person’s normal immune function? Psychological stress . i. Psychological stress is one of the factors that can depress a person’s normal immune function.

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3. Renal Disease a. A renal disease most often associated with autoimmunity is: Glomerulonephritis i. Glomerulonephritis is associated with autoimmunity 4. Autoimmune disease a. Autoimmunity is an alteration in the ability of the body to tolerate its own self-antigens. Under normal functioning, the immune system does not attack the individual’s own antigens. Especially with aging and even healthy individuals across the life span, individuals may produce small quantities of antibodies (autoantibodies) against their own antigens. The presence of a low number of autoantibodies does not automatically indicate the development of a full autoimmune disease. But autoimmune diseases may occur when the immune system overreacts again self-antigens to the extent that tissue damage occurs. The damage is caused by the autoantibodies and T-cells. Autoimmune diseases include: Rheumatoid Arthritis, Systemic Lupus Erythematosus, Multiple Sclerosis, and Sjogren’s Syndrome. Presenting clinical manifestations will depend on the area of the body affected. Regardless of the affected body area, autoantibodies and T- cells, and in some cases, B-cells, react in the associated body system to produce the characteristic signs and symptoms. b. Types of Autoimmune diseases i. Several autoimmune diseases are summarized below and includes the body areas affected and the specific immune system changes that occur. Autoimmune Disease Common Manifestations Immune System Changes Systemic Lupus Erythematosus Tissue inflammation, vasculitis, rash, tissue inflammation Autoantibodies and auto-active T-cells against DNA and nucleoprotein antigens Rheumatoid Arthritis Joint inflammation, stiffness and pain; loss of range of motion Autoantibodies and auto- reactive T-cells and B-cells against joint-associated antigens Multiple Sclerosis Formation of sclerotic plaque in the brain; leads to muscle weakness and ataxia Autoantibodies and auto- reactive T-cells and B-cells against joint-associated antigens Sjogren’s Syndrome Inflammation in salivary and lacrimal glands Autoantibodies and auto- reactive T-cells against apoptotic cells c. Ex: Clinical Application of Rheumatoid Arthritis i. B.P., a 56-year old female reports to the primary care clinic for a regular check- up. She tells the NP that she has been very tired lately, but attributes it to caring for her husband who was recently diagnosed with end stage renal failure. ii. She has been juggling teaching her high school students while also taking her husband to dialysis three times per week. She reports joint pain and tenderness in her fingers, especially on her thumbs along with bilateral stiffness, especially upon awakening. The stiffness seems to improve once she is at work, but she notices that she still feels stiff at times during the day.

iii. The NP conducts an exam and the subjective and objective findings reveal the following: 1. Subjective : painful and tender finger joints, stiffness of fingers upon awakening that improves with movement, fatigue 2. Objective : Swollen metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints, PIP joints warm to touch and red, rheumatoid nodule on the proximal ulna, decreased ROM of bilateral wrists and fingers. iv. B.P. is experiencing classic symptoms of inflammation in the synovial lining of the joints. The complement system is activated when the immune complexes deposit in the synovial tissue that results in the activation of complement. Other mediators that become involved include the kinins, prostaglandins and cytokines. The articular cartilage eventually breaks down because of the actions of the neutrophils and macrophages. They ingest the immune complexes that results in articular cartilage breakdown. Patients with RA will be treated with drugs in combination to reduce the inflammation. These include Disease- Modifying Antirheumatic Drugs (DMARDS), Glucocorticoids and NSAIDS. 5. Rheumatoid Arthritis a. Which of the following assessment findings would support a diagnosis of Rheumatoid Arthritis? swollen metacarpophalangeal joints i. The assessment findings of RA include swollen metacarpophalangeal joints. 6. Systemic lupus erythematosus a. Which of the following statements best describes the symptoms of SLE? Tissue inflammation, vasculitis, rash, tissue inflammation i. The symptoms of SLE include tissue inflammation, vasculitis, rash and tissue inflammation. 7. Immune Components a. The following immune components can be involved in autoimmune diseases: T-cells, B- cells, and autoantibodies. True i. Autoantibodies and T-cells, and in some cases, B-cells can be involved in autoimmune diseases 8. Low Autoantibodies a. The presence of a low number of autoantibodies is an indicator that the individual will develop an autoimmune disease. False i. The presence of a low number of autoantibodies does not automatically indicate the development of a full autoimmune disease

week 1 edapt notes

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