The nurse should recognize which response is the immune system's reaction to a source of inflammation?

A. Increase in interstitial osmotic pressure due to cellular damage. A crushing injury damages cells, leading to the release of intracellular proteins and solutes into the interstitial space. This increases interstitial osmotic pressure, drawing fluid from the blood vessels into the injured tissues, causing edema. The inflammatory response further contributes to capillary permeability and fluid leakage.
B. Decrease in interstitial pressures due to low blood pressure. Blood pressure does not directly regulate interstitial pressure in a localized trauma area. Even if systemic blood pressure were low, localized edema can still occur due to tissue damage and increased capillary permeability.
C. Increased intravascular osmotic pressure due to crushing injury. Osmotic pressure in the blood is primarily determined by plasma proteins, such as albumin. A crushing injury does not increase intravascular osmotic pressure; instead, it increases interstitial osmotic pressure, pulling fluid out of the blood vessels.
D. Increased intravascular hydrostatic pressure due to trauma. While trauma can cause localized vascular changes, hydrostatic pressure primarily affects systemic circulation. In this case, localized tissue damage and inflammation—not increased intravascular pressure—are responsible for edema formation.

A. Immediate allergic reaction mediated by sensitized mast cells. This describes a Type I hypersensitivity reaction, which is an immediate allergic reaction. It involves IgE antibodies and mast cell degranulation, leading to symptoms such as hives, anaphylaxis, and respiratory distress. Latex allergies can involve Type I reactions, but delayed hypersensitivity is a Type IV reaction.
B. Antigen-antibody complexes deposit in tissues activating inflammation. This describes a Type III hypersensitivity reaction, which involves immune complex deposition leading to inflammation, as seen in lupus or serum sickness. Latex allergies do not involve immune complex deposition.
C. T-cells sensitization initiates the macrophage release of cytokines causing a delayed reaction. This describes a Type IV hypersensitivity reaction, which is a delayed-type hypersensitivity (DTH) mediated by T-cells rather than antibodies. In latex-induced delayed hypersensitivity, T-cells recognize latex proteins and release cytokines, leading to localized skin inflammation, rash, and itching, typically 24–48 hours after exposure.
D. Antibodies are formed against antigens on cell surfaces. This describes a Type II hypersensitivity reaction, which involves antibody-mediated destruction of cells, as seen in hemolytic anemia or blood transfusion reactions. Latex allergies do not involve direct antibody attack on cells.