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Question #46865

Difficulty: 8/10 | 🟢 Free

The Question

In a state of severe, untreated insulin deficiency, a patient exhibits weakened cardiac contractility and altered myocardial conduction. Considering the structural and metabolic requirements of the cardiac syncytium, which of the following most accurately explains the cellular mechanism behind this physiological decline?

Options

  • A.

    Reduced glucose uptake diminishes ATP availability, impairing Na+/K+ ATPase activity and disrupting the electrochemical gradients required for rapid conduction through intercalated discs.

  • B.

    Excess glucagon competitively inhibits the binding of calcium ions to troponin-C, directly uncoupling excitation-contraction within the myocardial syncytium.

  • C.

    The absence of insulin triggers the structural closure of gap junctions in the intercalated discs to prevent the intercellular spread of toxic ketone bodies.

  • D.

    Myocardial cells shift entirely to anaerobic glycolysis, leading to lactic acidosis that physically degrades the desmosomes holding the myocytes together.

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Correct Answer

Step-by-Step Solution

Explanation

How the Examiner Thinks

Comparative_Analysis

Sharpen your ability to evaluate multiple scenarios and distinguish between competing potential answers.

Concepts Behind This Question

Intercalated Disc Function|Insulin vs Glucagon Effects|Regulation of Cardiac Activity

Why This Question Is Tricky

Common Mistakes

Conceptual Pivot: Linking endocrine metabolic regulation (insulin/glucose) to electrophysiology (ATP-dependent Na+/K+ pumps and intercalated discs).

Students often fail to recognize that the functional syncytium of the heart relies heavily on continuous ATP generation not just for contraction (myosin ATPase), but for maintaining the resting membrane potential necessary for gap junction-mediated conduction.

Quick Facts About This Question

Question Information

SubjectBiology
ChapterStructural Organisation in Animals - Class 11
ConceptIntercalated Disc Function
Difficulty8
Cognitive Load5
Target Solve Time120 sec
AccessFree