NR507NP Advanced Pathophysiology edapt week 1 With 100% correct answers + rationales 2026

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.

Clinical manifestations of hypersensitivity

Mast Cells

Mast 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.

Type III

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.

onset time, eczema, dog, outside, SOB, wheezing

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.

Production of autoantibodies targeting the thyroid-stimulating hormone receptor

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?

Graves Disease

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.

The pathophysiological processes of a type 3 immune complex hypersensitivity in the correct order are as follows:​

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

Poison Ivy contact dermatitis

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.

Allergic Rhinitis, asthma, Anaphylaxis

Type 1

Autoimmune hemolytic anemia, graves disease

Type II

SLE

Type III

Poison Ivy, latex exposure

Type IV

hemoglobin and hematocrit

Immediate follow up hypersensitivity case study.

In SLE anemia is due to

Autoimmunity

Dishcarge inst

For clients with type 3 immune-complex mediated reactions, such as systemic lupus erythematosus (SLE), antibodies are formed to antigens circulating in the blood, resulting in immune complexes that deposit in tissues. These immune complexes activate the complement system and neutrophil cells, causing inflammation and destroying the individual's own tissue. Clients with SLE have an increased risk of infection and must perform hand hygiene diligently.​

Iron supplements may also be needed to replenish iron stores. Iron supplementation's most frequent side effects include nausea and constipation, not diarrhea. The client should not stop taking their phenytoin while taking the oral corticosteroid medication. SLE has long-term hypersensitivity exacerbations and remissions, with currently no cure, only supportive care.

Case scenario presents with UTI sx

The nurse practitioner should order a urine culture and sensitivity to determine bacteremia. The client is clinically stable but symptomatic of a suspected urinary tract infection. Oral hydration should be recommended.​

After conducting a thorough health history, physical exam, and positive urine lab test (leukocyte esterase and nitrates in urine), the NP diagnoses the client with an uncomplicated urinary tract infection (UTI) and will advise the client to take the prescribed antibiotic and increase fluid intake to help flush out bacteria.​

History does not support evidence of an STI, the need for an abdominal ultrasound, or consulting a nephrologist.