A client who is experiencing respiratory distress is admitted with respiratory acidosis.

Which pathophysiological process supports the client's respiratory acidosis?

Drinking plenty of water whenever thirsty is not the most appropriate action for a patient with hypernatremia. While it's important to stay hydrated, excessive water intake can potentially worsen hypernatremia by diluting blood sodium levels further. This is because the body tries to balance sodium levels by either retaining water or excreting it through urine. In hypernatremia, the body is already short on water relative to sodium, so consuming too much water can exacerbate the imbalance.

Choice B rationale:

Reviewing food labels for sodium content is crucial for managing hypernatremia. It empowers patients to make informed choices and limit their sodium intake.

Sodium is a major contributor to hypernatremia, and reducing dietary sodium intake is a key strategy to lower blood sodium levels.

By carefully reading food labels and selecting low-sodium options, patients can effectively manage their sodium intake and promote a gradual return to normal sodium levels.

This approach addresses the root cause of hypernatremia and promotes long-term control of blood sodium levels.

Choice C rationale:

Monitoring daily urine output volume can be helpful in tracking fluid status, but it's not the primary action for managing hypernatremia.

While urine output can provide insights into fluid balance, it doesn't directly address the underlying issue of excessive sodium. Focusing on dietary sodium intake is a more direct and effective approach to correcting hypernatremia.

Choice D rationale:

Using salt tablets after strenuous exercise is not recommended for patients with hypernatremia.

Salt tablets are intended to replenish electrolytes lost through sweating, but they can worsen hypernatremia by further increasing sodium levels.

Patients with hypernatremia should focus on reducing sodium intake, not increasing it.

Choice A rationale:

Autoimmune responses occur when the immune system mistakenly attacks the body's own tissues. They are not typically triggered by allergens like bee stings.

Autoimmune responses often develop slowly over time and present with symptoms related to the specific tissues being attacked.

The rapid onset of symptoms in this case, along with the specific symptoms of rash, shortness of breath, and low blood pressure, are not characteristic of an autoimmune response.

Choice B rationale:

Type II hypersensitivity reactions involve antibodies that target and destroy cells or tissues. These reactions often take hours or days to develop, rather than minutes.

Examples of type II hypersensitivity reactions include transfusion reactions, hemolytic disease of the newborn, and some autoimmune diseases.

The rapid onset of symptoms in this case is not consistent with a type II hypersensitivity reaction.

Choice C rationale:

Cell-mediated hypersensitivity reactions involve T cells that directly attack cells or tissues. These reactions typically take 1-3 days to develop.

Examples of cell-mediated hypersensitivity reactions include contact dermatitis (e.g., poison ivy), graft-versus-host disease, and some drug reactions.

The rapid onset of symptoms in this case, as well as the specific symptoms of rash, shortness of breath, and low blood pressure, are not characteristic of a cell-mediated hypersensitivity reaction.

Choice D rationale:

IgE response hypersensitivity reactions are the most immediate type of allergic reaction.

They are mediated by immunoglobulin E (IgE) antibodies, which bind to mast cells and basophils.

When an allergen (like bee venom) cross-links IgE antibodies on mast cells, it triggers the release of histamine and other inflammatory mediators.

These mediators cause vasodilation, increased vascular permeability, smooth muscle contraction, and mucus secretion, leading to the characteristic symptoms of an allergic reaction.

The rapid onset of symptoms in this case, including rash, shortness of breath, and low blood pressure, are consistent with an IgE-mediated hypersensitivity reaction.