RML MAINS 2025
Medical & Surgical Nursing
Medium

Due to release of adrenocortical steroids by stress in patients who have undergone extensive prolonged surgery are likely to develop depletion of:

Appeared in: RML MAINS 2025

Explanation

  • Surgical stress activates the Hypothalamic-Pituitary-Adrenal (HPA) axis, leading to the release of adrenocortical steroids like cortisol and aldosterone.
  • Aldosterone, a mineralocorticoid, acts on the renal tubules to increase the reabsorption of sodium and water, which helps maintain blood pressure.
  • To maintain electrochemical balance during sodium retention, the kidneys increase the excretion of potassium ions into the urine.
  • This enhanced renal excretion of potassium is the primary cause of its depletion (hypokalemia) in the postoperative period following major stress.

Why Other Options Were Wrong

  • Option A: Adrenocortical steroids, specifically aldosterone, cause the kidneys to retain sodium, not deplete it. This is a key part of the body's mechanism to maintain blood volume during stress.
  • Option C: The acute hormonal response to surgical stress primarily affects sodium and potassium balance. Calcium levels are not directly or immediately depleted by this mechanism.
  • Option D: Chloride is an anion that typically follows the movement of sodium, a cation, to maintain electrical neutrality. Since sodium is retained, chloride is also generally retained, not depleted.

Related Visual

Visual explanation — Related Visual
Clinical Relevance
  • Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Pathophysiology of surgical stress and electrolyte imbalance as background academic context rather than a clinical decision trigger.
  • Nurses must diligently monitor postoperative patients for clinical signs of hypokalemia, including muscle weakness, fatigue, constipation or paralytic ileus, and cardiac arrhythmias.
  • ECG monitoring is crucial in at-risk patients, as hypokalemia can cause characteristic changes like flattened T waves, prominent U waves, and ST-segment depression, which can precede life-threatening arrhythmias.
  • What if the patient has pre-existing chronic kidney disease (CKD)? The answer would change significantly. A patient with CKD may be unable to excrete potassium effectively. The stress response would still occur, but the impaired kidneys might lead to a dangerous accumulation of potassium (hyperkalemia) instead of depletion, requiring a completely different management approach.
How to Approach the Question
  • First, identify the key elements in the question: 'extensive prolonged surgery' (a major stressor), 'release of adrenocortical steroids', and 'depletion' of an electrolyte.
  • Recall the body's physiological response to major stress, which involves the activation of the HPA axis and the release of stress hormones.
  • Focus on the function of the primary adrenocortical steroids involved: cortisol and, critically, aldosterone (a mineralocorticoid).
  • Remember the main action of aldosterone on the kidneys: it promotes the retention of sodium (and water) in exchange for the excretion of potassium.
  • Connect this action to the question's outcome: the excretion of potassium leads to its depletion in the body.
  • Evaluate the options based on this mechanism. Sodium is retained, not depleted. Calcium and chloride are not the primary electrolytes lost through this specific hormonal pathway.
Concept Tested & Keywords
  • Concept Tested: Pathophysiology of surgical stress and electrolyte imbalance
  • Stem keywords: adrenocortical steroids, stress, extensive prolonged surgery, depletion
  • Lead-in keywords: likely to develop depletion of
  • Negative lead-in flag: false

Question ID

QJNvu7RoNb4uUY78zOU-Ab

Reference Book

E6 Pharmacology KD Tripathi Essentials 9e Part 1 p. 332-334

E6 Pharmacology Nursing Lilley 11e Part 2 p. 223-225

E6 Pharmacology Katzung 16e p. 1107-1109

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