What is the common factor for etiology and pathophysiology of folliculitis, furuncles, and carbuncles?

A. Cool the burn with ice water:

Not recommended: Cooling a burn with ice water directly is not recommended as it can lead to further tissue damage and complications. Instead, the burn should be cooled with cool (not cold) running water for a limited time and then covered with a clean, dry cloth.

B. Administer opioid analgesics:

Recommended: Severe burns can cause excruciating pain, and opioid analgesics are often necessary to manage this pain effectively. However, the specific opioid, dosage, and route of administration should be determined by the healthcare provider based on the client's condition and pain level.

C. Administer systemic antibiotics:

Not routinely recommended: Unless there are signs of infection or the burn involves deep tissue damage, systemic antibiotics are not typically administered prophylactically for burn injuries. However, if there are signs of infection, such as redness, swelling, warmth, or drainage from the burn site, antibiotic therapy may be initiated based on culture and sensitivity results.

D. Administer benzodiazepines for anxiety management:

Considered: Severe burns can cause significant psychological distress and anxiety in patients. Benzodiazepines may be considered to manage acute anxiety and agitation in these situations. However, the decision to administer benzodiazepines should be made based on the client's overall condition, vital signs, and response to non-pharmacological interventions for anxiety.

E. Lay the head of the bed flat:

Not recommended: In a client with severe burns who is experiencing increased work of breathing, anxiety, and rapid breathing, it is generally more beneficial to elevate the head of the bed slightly (semi-Fowler's position) to improve respiratory mechanics and reduce anxiety-related respiratory distress.

A. Diabetic ketoacidosis (DKA) in a person with emphysema:

In DKA, there is typically metabolic acidosis due to the accumulation of ketones in the blood, leading to a decrease in pH. However, the respiratory compensation mechanism in DKA usually results in a decreased PaCO2 (respiratory alkalosis) rather than an elevated PaCO2 as seen in the blood gas values provided. Additionally, emphysema is associated with chronic respiratory acidosis, not respiratory alkalosis as indicated by the elevated PaCO2.

B. Diarrhea for 36 hours in an older, frail woman:

Prolonged diarrhea can lead to metabolic acidosis due to the loss of bicarbonate through the gastrointestinal tract. The pH of 7.12 and the decreased HCO3- (22 mEq/L) suggest metabolic acidosis. However, the elevated PaCO2 (respiratory acidosis) is not consistent with pure metabolic acidosis caused by diarrhea. Respiratory acidosis typically occurs due to hypoventilation or respiratory dysfunction.

C. Anxiety-induced hyperventilation in an adolescent:

Anxiety-induced hyperventilation can lead to respiratory alkalosis due to excessive blowing off of CO2, resulting in a decrease in PaCO2. The pH of 7.12 is consistent with acidosis, but the elevated PaCO2 contradicts respiratory alkalosis. Anxiety-induced hyperventilation would typically result in a higher pH and lower PaCO2.

D. Bronchial obstruction related to aspiration of a hot dog:

A bronchial obstruction causing inadequate ventilation can lead to respiratory acidosis due to CO2 retention. The pH of 7.12 and the elevated PaCO2 (65 mm Hg) indicate respiratory acidosis. This situation is consistent with the blood gas values provided.