A patient with liver cirrhosis and ascites is being assessed. Which of the following physiological changes is… - NORCET 10 Prelims-2026

NORCET 10 Prelims-2026

Medical & Surgical Nursing

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Appeared in: NORCET 10 Prelims-2026

Explanation

In liver cirrhosis, extensive scarring (fibrosis) obstructs blood flow through the portal vein.
This obstruction leads to a significant increase in pressure within the portal venous system, a condition known as portal hypertension.
Therefore, a decrease in portal pressure is the opposite of what occurs and is not an expected finding.

Option A: Increased ADH secretion is an expected compensatory mechanism in cirrhosis. Splanchnic vasodilation and ascites lead to a reduced effective circulating volume, which stimulates ADH release to promote water retention.
Option B: Increased hepatic venous pressure is an expected finding. The fibrotic and nodular liver structure obstructs blood outflow, leading to an increase in pressure within the hepatic veins (post-sinusoidal obstruction).
Option D: Increased aldosterone is an expected finding. The perceived low blood volume triggers the Renin-Angiotensin-Aldosterone System (RAAS), leading to increased aldosterone secretion. This causes the kidneys to retain sodium and water, contributing to ascites.

Visual 1: Flowchart - A flowchart illustrating the pathophysiology of ascites formation in cirrhosis. It would start with liver fibrosis, leading to portal hypertension, then branching to show splanchnic vasodilation, RAAS activation (increased aldosterone), and increased ADH, all culminating in sodium/water retention and fluid accumulation in the peritoneum.
Visual 2: Diagram - A diagram comparing a healthy liver with a cirrhotic liver. The cirrhotic liver diagram would show fibrosis and nodularity, with arrows indicating obstructed blood flow in the portal vein and hepatic vein, visually explaining the pressure increases.

Clinical Relevance

Nursing practice connection: Use the key finding related to Pathophysiology of ascites in liver cirrhosis to guide bedside assessment, documentation, and the next nursing action.
Understanding the pathophysiology of ascites is crucial for nursing management, which includes monitoring fluid status (daily weights, abdominal girth), administering diuretics (like spironolactone, an aldosterone antagonist), and enforcing sodium restriction.
Nurses must monitor for complications of portal hypertension, such as bleeding from esophageal varices, which is a medical emergency.
Patient education is key, focusing on dietary restrictions (low sodium), medication adherence, and recognizing signs of worsening ascites or complications like spontaneous bacterial peritonitis (fever, abdominal pain).

How to Approach the Question

First, identify the core concept: the physiological consequences of liver cirrhosis and ascites.
Note the negative framing of the question: it asks what is 'not expected'. This means three of the options will be expected findings, and one will be incorrect.
Recall the hallmark feature of cirrhosis: fibrosis leading to obstruction of blood flow.
Consider how this obstruction affects pressures. It increases resistance, so pressures behind the obstruction (portal vein) and within the obstructed organ (liver/hepatic vein) must increase.
Evaluate the body's compensatory responses. The fluid shift (ascites) and vasodilation lead to a perceived 'low volume' state, which activates hormonal systems like RAAS (aldosterone) and ADH to retain salt and water.
Review each option against this pathophysiological model. Increased ADH, increased hepatic venous pressure, and increased aldosterone are all consistent. Decreased portal pressure directly contradicts the primary pathology of portal hypertension.

Concept Tested & Keywords

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