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Question #45386
The Question
A full-term pregnant female experiences a normal fetal ejection reflex and exhibits adequate maternal oxytocin levels, yet her uterine contractions remain extremely weak, leading to prolonged labor. Blood tests reveal a specific endocrine disorder affecting mineral metabolism. Which of the following underlying conditions best explains the failure of the myometrium to contract, and what is the precise physiological mechanism disrupted?
Options
- A.
Hyposecretion of Parathyroid Hormone (PTH); failure of the Ca2+-Calmodulin complex to activate Myosin Light Chain Kinase (MLCK).
- B.
Hypersecretion of Thyrocalcitonin (TCT); failure of Ca2+ to bind Troponin-C and unmask myosin-binding sites on actin.
- C.
Hyposecretion of Fetal Cortisol; inability to upregulate oxytocin receptors on the myometrial surface.
- D.
Hypersecretion of Parathyroid Hormone (PTH); excessive efflux of Ca2+ from the sarcoplasmic reticulum causing premature muscle fatigue.
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
Ca2+_Calmodulin_Complex|Myometrial_Contraction|PTH_Calcitonin
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: This question bridges Reproductive Neuroendocrinology with Chemical Coordination (Calcium Homeostasis) and Locomotion (Muscle Contraction).
The primary trap (Option B) exploits a common misconception: students frequently apply the skeletal muscle contraction mechanism (Ca2+ binding to Troponin-C) to all muscle types, failing to recognize that the myometrium is smooth muscle and strictly utilizes the Ca2+-Calmodulin-MLCK pathway.
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Human Reproduction - Class 12 |
| Concept | Parturition Neuroendocrine Reflex |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |