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Exam (elaborations)

Coagulation Disorders (HEME-301) | 100 Exam Questions on Hemostasis, Hemophilia, DIC & Coagulation Pathways

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This document provides 100 structured exam questions with precise and well-explained answers focusing on coagulation disorders, part of the HEME-301 course at the University of Health Sciences for the 2025/2026 academic year. It covers both primary and secondary hemostasis in depth, from platelet adhesion to clot stabilization, with special emphasis on coagulation factor deficiencies, von Willebrand disease, hemophilias, and DIC. Topics Covered: Primary & Secondary Hemostasis: Primary hemostasis involves platelet adhesion (via GPIb-vWF), activation (ADP → GPIIb/IIIa expression), and aggregation (fibrinogen bridge) Secondary hemostasis: clot stabilization via coagulation cascade, initiated by intrinsic (factor XII) and extrinsic (factor VII) pathways Coagulation Pathways & Factors: Intrinsic: XII → XI → IX (+VIII) → X Extrinsic: Tissue factor (III) → VII → X Common pathway: X (+V) → II (thrombin) → I (fibrin) → cross-linked by XIII Regulation by Protein C & S, Vitamin K–dependent factors (II, VII, IX, X), and lab measurement through PT (extrinsic) and PTT (intrinsic) Key Disorders and Inheritance Patterns: Hemophilia A – Factor VIII deficiency, X-linked recessive Hemophilia B – Factor IX deficiency, X-linked recessive Hemophilia C – Factor XI deficiency, autosomal recessive Severity classified by residual factor activity: • Mild: 6–10% • Moderate: 2–5% • Severe: <1% von Willebrand Disease (vWD): Type 1: Quantitative partial deficiency (~80%) Type 2: Qualitative defect Type 3: Complete absence of vWF Diagnosis via ristocetin cofactor assay, importance in factor VIII stabilization, and treatment with desmopressin (DDAVP) Fibrinolysis & Anticoagulants: Plasmin: cleaves fibrin but not cross-linked D-dimers Activated by tPA, inhibited by PAI and α2-antiplasmin Vitamin K activation by epoxide reductase in the liver, essential for γ-carboxylation of clotting factors Disseminated Intravascular Coagulation (DIC): Consumptive coagulopathy triggered by sepsis, trauma, obstetric complications, malignancy, transfusions, etc. (mnemonic: STOP Making New Thrombi) Leads to platelet and clotting factor depletion → bleeding and microvascular thrombosis This high-yield resource is suitable for: Medical students studying hematology, internal medicine, or preparing for practical exams Candidates preparing for USMLE Step 1 & 2, PLAB, AMC, COMLEX, and clinical rotations Nursing, pharmacy, and clinical lab science students reviewing coagulation mechanisms and disorders With clear diagrams, mechanisms, and Q&A format, this resource makes mastering coagulation disorders efficient and clinically relevant. Keywords: hemostasis, platelet plug, GPIb, GPIIbIIIa, von Willebrand factor, coagulation cascade, PT, PTT, hemophilia A, hemophilia B, factor VIII, factor IX, ristocetin assay, vitamin K, protein C, protein S, thrombin, fibrin, DIC, fibrinolysis, tPA, α2-antiplasmin, bleeding disorders, clotting factors

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Institution
Coagulation Disorders
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Coagulation Disorders

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Uploaded on
December 12, 2025
Number of pages
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Written in
2025/2026
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HEME: Dr. Hayes Coaggulation
Disorders 2025/2026 Exam Questions
and Answers | 100% Pass



Primary Hemostasis - 🧠ANSWER ✔✔platelet form a weak platelet plug at

the site of injury


Secondary Hemostasis - 🧠ANSWER ✔✔clotting factors, from the liver, aid

in stabilizing the clot

*Where is von Willebrand's Factor (vWF) stored in endothelial cells -

🧠ANSWER ✔✔weibel-palade bodies


*Where is von Willebrand's Factor (vWF) stored in platelets - 🧠ANSWER

✔✔alpha granules

, What molecule do endothelial cells produce from arachidonic acid -

🧠ANSWER ✔✔PGI2 (ANTI-coaggulation)


What molecule do platelets produce from arachidonic acid - 🧠ANSWER

✔✔TXA2 (pro-coaggulation)


in response to endothelial injury, vWF spans the lumen of the endothelium

to bind to - 🧠ANSWER ✔✔subendothelial collagen


primary hemostasis adhesion - 🧠ANSWER ✔✔GPIb on platelets bind to

vWF


primary hemostasis activation - 🧠ANSWER ✔✔platelets (ADP activation)

begin to express GPIIbIIIa (linkers on platelets)


primary hemostasis aggregation - 🧠ANSWER ✔✔fibrinogen binds to

GPIIbIIIa between platelets, forming the weak platelet plug


factor 12 is activated by - 🧠ANSWER ✔✔negatively charged subendothelial

collagen


factor 11 is activated by - 🧠ANSWER ✔✔factor 12a


factor 9 is activated by - 🧠ANSWER ✔✔factor 11a

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