NR507 week 1 edapt guide updated version, Study Guides, Projects, Research of Nursing

Download NR507 week 1 edapt guide updated version and more Study Guides, Projects, Research Nursing in PDF only on Docsity!

NR507 week 1 edapt guide updated

version

Advanced Pathophysiology

Week 1:Edapt Notes

-Immediate hypersensitivity is mediated by IgE antibodies, which resulting 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.

1. are the primary effector cells and are responsible for initiating and mediating hypersensitivity reactions.

• Mast cells, type 1 characterized by the rapid release of proinflammatory mediators like histamines, leukotrienes, and cytokines in response to allergen exposure, mast cells are the primary effector cells responsible for initiating and mediating type 1 hypersensitivity reactions.

1. hypersensitivity reactions involve the formation of that can deposit in tissues, leading to complement activation, inflammation, and tissue destruction. -Type 3, immune complexes

• 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. Type 1 = Mediated by IgE antibodies

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

A type 3 reaction is mediated by immune complexes.

Type 4 = 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 A type 4 delayed reaction is mediated by cellular response.

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

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 she might “leak.” She tells the NP that she suspects that she has a UTI. She reported that is 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 diagnosed the client with uncomplicated UTI and orders a course of sulfamethoxaole/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, 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

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

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).

Graves’ disease symptoms include bulging eyes, enlarged thyroid (goiter), arrhythmia and tachycardia, nausea and diarrhea, tremor, change in menstrual cycles (in females), muscle weakness, headache, weight loss, anxiety and irritability, and increased perspiration. 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 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.

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

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.

• 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. Your response is correct! 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

Anaphylaxis is caused by the body's immune response to an allergen. Allergens are harmless substances that cause an overreaction response in some individuals. Common allergens include foods such as nuts or shellfish, certain medications, insects, or latex. When a person with an allergy comes in contact with their allergen trigger, white blood cells, such as mast cells, released during anaphylaxis is histamine. Histamine causes the dilation of blood vessels and increases heart rates 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

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. Allergic rhinitis = 1 Asthma =