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Question #46357
The Question
In a severe case of Erythroblastosis fetalis, massive destruction of fetal erythrocytes by maternal antibodies can occasionally lead to a paradoxical state of severe internal hemorrhaging. Which of the following best explains the physiological basis of this hemorrhagic complication?
Options
- A.
Maternal anti-Rh antibodies directly cross-react with fetal megakaryocytes, causing severe immune thrombocytopenia.
- B.
Massive hemolysis releases intracellular pro-coagulants, triggering widespread intravascular clotting that depletes circulating clotting factors.
- C.
Excess bilirubin from lysed erythrocytes competitively inhibits the conversion of prothrombin to thrombin in the clotting cascade.
- D.
Severe hypoxia from fetal anemia induces the liver to synthesize endogenous heparin instead of fibrinogen.
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
ABO-Rh Incompatibility Logic|Clotting Cascade Factors
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Students typically associate Erythroblastosis fetalis strictly with anemia and jaundice (direct NCERT facts).
The trap is failing to connect massive cellular lysis with the release of pro-coagulants.
The core misconception addressed is that hemorrhaging is always caused by an initial inability to clot; here, it is paradoxically caused by over-activation and subsequent exhaustion of the clotting cascade (consumptive coagulopathy).
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Body Fluids and Circulation - Class 11 |
| Concept | ABO-Rh Incompatibility Logic |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |