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Question #45442
The Question
A patient suffering from severe hepatic cirrhosis presents with chronic hypotension and a reduced Glomerular Filtration Rate (GFR). Blood analysis reveals abnormally elevated levels of Renin. Despite this hyper-reninemia, the patient's blood pressure fails to normalize. Which of the following best explains the primary physiological bottleneck in the Renin-Angiotensin-Aldosterone System (RAAS) in this scenario?
Options
- A.
Inadequate hepatic synthesis of angiotensinogen creates a substrate-limited state, preventing renin from generating Angiotensin I.
- B.
Hepatic dysfunction impairs the secretion of Angiotensin Converting Enzyme (ACE), halting the conversion of Angiotensin I to Angiotensin II.
- C.
Elevated renin levels induce a paradoxical negative feedback on the adrenal cortex, suppressing aldosterone secretion.
- D.
Decreased hepatic clearance of aldosterone leads to receptor downregulation in the distal convoluted tubule, causing obligate sodium loss.
Check Your Answer
Correct Answer
Step-by-Step Solution
Explanation
How the Examiner Thinks
Regulatory_Failure
Understand how NOT, EXCEPT, and logical constraints are used to manipulate exam results.
Concepts Behind This Question
Hormone_Half_life_Logic|Renin|Angiotensinogen
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Students often memorize the RAAS pathway linearly and associate its failure solely with kidney (JG cells) or lung (ACE) dysfunction.
They overlook the critical NCERT fact that Angiotensinogen is a plasma protein.
The trap is failing to recognize the enzyme-substrate kinetics: an enzyme (Renin) is functionally useless without its specific substrate (Angiotensinogen), making the liver an indispensable organ in renal blood pressure regulation.
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Chemical Coordination and Integration - Class 11 |
| Concept | RAAS Mechanism |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |