Medical Science 2025 Paper I 50 marks Describe

Q6

(a) (i) Describe the approach to laboratory diagnosis of chronic myeloid leukemia – chronic phase. 10 marks (ii) Describe the gross and light microscopic changes evolved over two weeks duration in myocardial infarction. Add a note on the role of serum cardiac biomarkers in the diagnosis of myocardial infarction. 5+5=10 marks (b) (i) Explain why beta blockers should not be given to diabetes patients who are on oral hypoglycaemic agents. 5 marks (ii) Explain why folic acid is given with methotrexate. 5 marks (c) (i) A 12-year-old child developed fever with multiple crops of vesicular rash starting from the face spreading towards the trunk. (I) Mention the mode of transmission and spread of the probable viral agent. Prepare a flowchart of the course of the infection in humans. Mention three tests for laboratory diagnosis of the agent. (II) Discuss the post-exposure preventive strategies. 5+5=10 marks (ii) Enumerate the malarial parasites prevalent in India. Of them, which species is notoriously associated with life-threatening complications ? What are the different characteristic peripheral blood smear findings in different species of parasites that cause malaria ? 10 marks

हिंदी में प्रश्न पढ़ें

(a) (i) चिरकाली मज्जाम श्वेतरक्तता के चिरकाली चरण में प्रयोगशाला निदान के अभिगम (अप्रोच) का वर्णन कीजिए। 10 (ii) हृदपेशी रोधगलन में दो सप्ताह की अवधि में विकसित होने वाले सकल तथा प्रकाश सूक्ष्मदर्शीय परिवर्तनों का वर्णन कीजिए। हृदपेशी रोधगलन के निदान में सीरम हृद बायोमार्कर्स की भूमिका पर टिप्पणी भी लिखिए। 5+5=10 (b) (i) स्पष्ट कीजिए कि डायबिटीज के उन रोगियों को जो मुख्य हाइपोग्लाइसीमिक एजेंट ले रहे होते हैं, बीटा-ब्लॉकर्स क्यों नहीं दिए जाने चाहिए। 5 (ii) स्पष्ट कीजिए कि मेथोट्रेक्सेट के साथ फोलिक एसिड क्यों दिया जाता है। 5 (c) (i) एक 12-वर्षीय बालक को ज्वर होने के साथ-साथ चेहरे से शुरू होकर धड़ तक फैल रही बार-बार पुनरावृत्ति कर रही वायुकोशीय पित्तिकाओं की उपज हो रही है। (I) संभावित विषाणु कारक के संचरण तथा प्रसार की प्रणाली क्या है, उल्लिखित कीजिए। मनुष्यों में संक्रमण की प्रक्रिया (कोर्स) का प्रवाह संचित्र बनाइए। कारक के प्रयोगशाला में निदान करने की तीन जाँचों को उल्लिखित कीजिए। (II) इस ऋणता में अनावरण-पश्चात् कौन-सी निवारण रणनीतियाँ अपनाई जा सकती हैं ? विवेचना कीजिए। 5+5=10 (ii) भारत में पाए जाने वाले मलेरिया परजीवियों के नाम गिनाइए। उनमें से कौन-सी परजीवी जाति प्राण-घातक जटिलताएँ प्रेरित करने के लिए कुख्यात है ? परिसरिय रक्त आलेप पर विभिन्न मलेरिया परजीवियों की जातियों के क्या-क्या भिन्न विशिष्ट परिणाम पाए जाते हैं ? 10

Directive word: Describe

This question asks you to describe. The directive word signals the depth of analysis expected, the structure of your answer, and the weight of evidence you must bring.

See our UPSC directive words guide for a full breakdown of how to respond to each command word.

How this answer will be evaluated

Approach

The directive 'describe' demands systematic, detailed exposition of laboratory methods, pathological changes, and clinical reasoning. Allocate approximately 20% (10 marks) to CML diagnosis, 20% (10 marks) to MI evolution and biomarkers, 20% (10 marks) to pharmacology explanations, 25% (12.5 marks) to varicella with flowchart and prevention, and 15% (7.5 marks) to malaria species and smear findings. Structure as: brief introduction → part-wise detailed description with sub-headings → integrated conclusion emphasizing clinical application.

Key points expected

  • CML chronic phase: peripheral smear showing leukocytosis with left shift, basophilia, low LAP score, t(9;22) BCR-ABL1 by FISH/PCR, bone marrow hypercellularity with granulocytic hyperplasia
  • MI 2-week evolution: gross changes from coagulative necrosis to yellow-brown softening; microscopic progression from neutrophilic infiltration to granulation tissue and early scar; cardiac biomarkers (troponin I/T, CK-MB) with their temporal windows
  • Beta-blockers in diabetes: masking of hypoglycemia symptoms (tremors, tachycardia), prolonged hypoglycemia by blocking glycogenolysis, interference with recovery from insulin-induced hypoglycemia
  • Folic acid with methotrexate: rescue of normal cells via competitive inhibition of dihydrofolate reductase, prevention of mucositis and bone marrow suppression while maintaining anti-tumor effect
  • Varicella: airborne/droplet transmission, centripetal rash distribution; flowchart showing incubation (10-21 days) → prodrome → vesicular rash → crusting; Tzanck smear, PCR, direct fluorescent antibody; post-exposure VZIG within 96 hours and vaccine
  • Malaria in India: P. vivax, P. falciparum, P. malariae, P. knowlesi (emerging); P. falciparum causes cerebral malaria/blackwater fever; smear differences: vivax (enlarged RBC, Schüffner's dots, amoeboid trophozoite), falciparum (multiple rings/cell, banana gametocytes, no enlargement), malariae (band form, rosette schizonts)

Evaluation rubric

DimensionWeightMax marksExcellentAveragePoor
Concept correctness25%12.5Precisely states BCR-ABL1 fusion gene mechanism, accurate MI histological timeline with specific days for each change, correct pharmacological rationale for beta-blocker contraindication and folate rescue, accurate varicella virology and malaria species identification with correct morphological detailsGenerally correct concepts but minor errors in gene nomenclature (e.g., 'Philadelphia chromosome' without specifying t(9;22)), vague MI timeline, incomplete explanation of folate rescue mechanism, confusion between malaria species morphologyFundamental errors such as describing CML as lymphoid proliferation, incorrect MI evolution sequence, wrong mechanism for beta-blocker interaction, confusing varicella with smallpox, or misidentifying P. vivax as causing cerebral malaria
Clinical correlation20%10Links CML findings to clinical presentation (splenomegaly, constitutional symptoms), connects MI pathology to clinical complications (ventricular aneurysm, rupture), explains real-world diabetes management implications, contextualizes varicella in Indian pediatric population, relates P. falciparum complications to endemic mortalityMentions clinical features without integrating with laboratory/pathological findings, superficial connection between pharmacology and patient outcomes, generic statements about disease burdenNo clinical context provided, purely theoretical description without patient-oriented application, or irrelevant clinical associations
Diagram / pathway20%10Clear, labeled flowchart of varicella infection course with timeline; well-drawn MI microscopic progression diagram; schematic representation of folate rescue mechanism; accurate malaria parasite morphology sketches with comparative featuresBasic flowchart without temporal precision, incomplete diagrams, or text-heavy description without visual aid where requiredMissing mandatory varicella flowchart, no diagrams for MI evolution, or incorrect schematic representations that mislead understanding
Differential / staging15%7.5Distinguishes CML chronic phase from accelerated/blast crisis using WHO criteria; differentiates MI from myocarditis histologically; contrasts varicella with smallpox (centrifugal vs centripetal, synchronous vs asynchronous rash); stages malaria severity criteriaMentions phases without specific criteria, superficial differential diagnosis, or incomplete staging informationNo differentiation between disease phases, confuses varicella with other vesicular exanthems, or fails to mention CML disease progression criteria
Management / public-health angle20%10Comprehensive post-exposure varicella prophylaxis (VZIG timing, vaccine, chemoprophylaxis for high-risk); detailed malaria control strategies (IRS, ITNs, ACT per NVBDCP guidelines); CML tyrosine kinase inhibitor therapy mention; evidence-based biomarker-guided MI managementGeneric prevention statements without specific timelines or national program references, standard treatment mentions without public health integrationNo preventive strategies for varicella, missing national malaria control program references, or completely omitting management aspects

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