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Question #45424
The Question
A somatic gain-of-function mutation in the TSH receptor gene of thyroid follicular cells causes constitutive activation of its intracellular signaling pathway, effectively acting as an oncogenic driver. In a patient with this specific mutation, which of the following physiological states is expected?
Options
- A.
High circulating T3 and T4 levels will exert strong negative feedback, leading to suppressed TSH and subsequent atrophy of the thyroid gland.
- B.
The thyroid gland will exhibit autonomous hormonogenesis and cellular proliferation despite undetectable levels of circulating TSH.
- C.
The anterior pituitary will secrete excessive TSH due to the continuous positive feedback from the hyperactive follicular cells.
- D.
The hypothalamus will upregulate TRH secretion to compensate for the rapid peripheral consumption of T3 and T4 by the proliferating cells.
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
TSH_Receptor|Thyroid_Follicles|Oncogenes vs Proto-oncogenes
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Students often associate thyroid gland proliferation (goiter/nodules) strictly with high TSH levels (as seen in iodine deficiency).
The trap is failing to recognize that a constitutively active mutated receptor bypasses the need for TSH, driving autonomous growth while simultaneously suppressing endogenous TSH via intact central negative feedback.
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Chemical Coordination and Integration - Class 11 |
| Concept | Thyroid Hormone Synthesis |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |